Comprehensive Physiology Wiley Online Library
For Librarians For Authors Editors About

Circulatory Correlates: Vascular Impedance, Resistance, and Capacity

Barry S. Gow

10.1002/cphy.cp020214

Source: Supplement 7: Handbook of Physiology, The Cardiovascular System, Vascular Smooth Muscle

Originally published: 1980

Published online: January 2011

Full Article on Wiley Online Library



Abstract

The sections in this article are:

1 Windkessel Vessels
1.1 Arterial Diameter Measurement
1.2 Caliber Changes and Hemodynamic Consequences in Windkessel Vessels
1.3 Arterial Elasticity and Hemodynamics
1.4 Effects of Alterations in Vasomotor Tone on Arterial Elasticity
1.5 Effects of Alterations in Transmural Pressure on Arterial Elasticity
1.6 Vasomotor Changes and Vascular Impedance
1.7 Smooth Muscle and Baroreceptor Areas
2 Resistance Vessels
2.1 Blood Flow, Pressure Gradient, Vascular Caliber, and Viscosity
2.2 Critical Closure
2.3 Vasomotor Changes in Microcirculation and Capillary Fluid Dynamics
2.4 Integrated Responses
3 Capacitance Vessels
3.1 Venoconstriction and Venous Capacity
3.2 Mobilization of Volume by Systemic Circulation: Venomotor Changes and Mean Circulatory Pressure
3.3 Mobilization by Regional Circulations
3.4 Changes in Compliance and Hemodynamic Consequences
3.5 Venomotor Changes and Cardiac Output
3.6 null
Figure 1. Figure 1.

effect of section of lumbar sympathetic trunk at L3−L4 on outside diameter (D) of dog femoral artery.

effect of stimulation of the lumbar sympathetic trunk at a level of L3−L4 on the outside diameter of a dog femoral artery. Stimulus parameters: 4.2 V, 5 ms, at 15 Hz. [From Gerová and Gero 102, by permission of the American Heart Association, Inc.]
Figure 2. Figure 2.

Equilibrium between internal (Pi) and external (Po) pressures and mean wall tension (T), which would have to be applied to both halves of longitudinally split, hollow cylinder to hold halves together.
Figure 3. Figure 3.

Elastic moduli (E) of relaxed and constricted carotid artery as function of strain and pressure, derived by Dobrin and Rovick from pressure‐circumference curves. At any pressure, E (constricted) < E (relaxed). “Unstressed” circumference of constricted vessel was used to compute strain for both constricted and relaxed vessels, leading to erroneous conclusion that at comparable strain, constricted vessels have lower elastic moduli. Compare this to same data plotted in Fig. 4 using appropriate “unstressed” circumferences to compute strain.

From Dobrin and Rovick 76
Figure 4. Figure 4.

Stress‐strain relationships of relaxed and constricted carotid artery derived from data of Dobrin and Rovick 76. Strain was calculated for each by using appropriate “unstressed” circumferences obtained at pressures of approximately 5 mmHg. At most strain and stress values and at comparable distending pressures, slope of stress‐strain curve is lower, that is, elastic modulus is lower for constricted vessel.
Figure 5. Figure 5.

Dependence of dynamic elastic modulus on arterial pressure. DTA, descending thoracic aorta; ABA, abdominal aorta; BCA, brachiocephelic artery; LSC, left subclavian artery; CA, carotid artery; FA, femoral artery. Note relatively greater pressure dependence of elasticity in peripheral arteries.

From Cox 64
Figure 6. Figure 6.

Pressure‐radius relationships for rabbit ear artery, showing little change in ΔP/Δro within normal range of arterial pressure despite very different degrees of vascular smooth muscle contraction. Curves are fully constricted (closed circles), intermediately constricted (closed squares), and fully relaxed (open and closed triangles). Epinephrine and a 60‐min period of electrical stimulation at 4 Hz were used to produce full or partial constriction. Open circles show response of artery to increasing pressure after electrical stimulation but without added epinephrine.
Figure 7. Figure 7.

Vascular input impedance (modulus and phase) of systemic circulation of dog plotted against frequency. Note relatively stable impedance modulus at frequencies above that of resting heart rate (2 Hz). This should be compared to higher values between 0 and 2 Hz and modulus of input impedance of simple elastic tube terminated by hydraulic resistance (Fig. 8 A). (Coherence is a measure of association between the variables and is akin to a correlation coefficient.

From Taylor 278, by permission of the American Heart Association, Inc
Figure 8. Figure 8.

Top: input impedance of branching assembly of elastic tubes (solid line) compared with that of single “equivalent” tube (broken line). Reflection coefficient is 0.6 in both cases, so that |Z0|0 at zero frequency is 11.5. Note reduction of modulus spikes, hence a greater stability of |Z0|0 when multiple tubes are present in model. Bottom: input impedance of random‐length, branching assembly as in Top, showing stabilizing effects on both modulus and phase of viscous properties (largely of smooth muscle) of vessel walls. Solid line shows no viscosity, dashed line represents phase angle of 10° for viscoelastic modulus, and dotted line shows phase angle of 20°. Results of wall viscosity are similar to fluid viscosity, except that latter elevates impedance modulus at zero frequency (i.e., input resistance).

From Taylor 277
Figure 9. Figure 9.

Mean systemic input impedance modulus and phase for 12 unanesthetized dogs before (open circles) and following (closed circles) carotid sinus hypotension produced by occlusion of brachiocephalic artery. Note increase in characteristic impedance, part of which may be due to elevated systemic pressure and its effect on elasticity, and part due to reduction cross‐sectional area of arterial tree.

From Cox et al. 67
Figure 10. Figure 10.

Effect of elevated blood pressure induced by norepinephrine injection on systemic vascular input impedance. Note shift to right of minima of modulus from roughly 3 and 8 Hz to 5 and 10 Hz, respectively. Failure of characteristic impedance to rise suggests that pressure‐induced increases in elasticity of arterial tree were offset by increases in its cross‐sectional area.

From O'Rourke and Taylor 219, by permission of the American Heart Association, Inc
Figure 11. Figure 11.

Vascular impedance of dog femoral artery showing effects of vasodilatation on modulus and phase. Reduction in reflection coefficient flattens undulations in modulus and phase. Shift to left of impedance modulus minimum is not completely explained by the random tube model 277,218, but such a disparity might be expected to arise from geometric dissimilarities between model and femoral vascular bed. Intercept of phase on frequency axis was variable—intercept during dilatation occurred at lower frequencies and supported model 277,218, whereas in later study 218 it occurred at a higher frequency than the control.

From Taylor 278, by permission of the American Heart Association, Inc
Figure 12. Figure 12.

Changes in contour and timing of peaks of simultaneously recorded femoral pressure waves and flow waves following vasodilatation induced by close arterial injection of acetylcholine. Note close correspondence of pressure and flow during dilatation, which can be anticipated when reflections are substantially reduced. Mean blood pressure: 107 mmHg (control), 94 mmHg (vasodilated). Mean flow: 1.08 ml/s (control), 6.93 ml/s (vasodilated).

From O'Rourke and Taylor 218, by permission of the American Heart Association, Inc
Figure 13. Figure 13.

Modulus of vascular impedance of systemic circulation and impedance of renal, celiac, and femoral vascular beds under control conditions (open circles), reflex constriction (solid squares), and reflex dilatation (solid triangles) before and after bilateral vagotomy. In renal and celiac beds, vasoconstriction elevated impedance and vasodilatation reduced impedance at all frequencies, although this was true only for first four harmonies in femoral bed.

From Cox and Bagshaw 66, by permission of the American Heart Association, Inc
Figure 14. Figure 14.

Changes in relative contribution of oscillatory power to total cardiac power (oscillatory power fraction) as function of heart frequency, and influence on control relationship (open circles) of isoproterenol (uppermost curve, open squares), norepinephrine (solid circles), and angiotensin (lowest curve, closed squares). Isoproterenol elevated cardiac output and total cardiac power but increased pulsatile losses, thereby reducing cardiac efficiency.

From Cox 62
Figure 15. Figure 15.

Profile of pressure drops through systemic circulation, demonstrating major site of vascular resistance in precapillary vessels and showing increase and decrease in capillary pressure, which occurs during precapillary vasodilatation and vasoconstriction, respectively.

From Keele and Neil 163
Figure 16. Figure 16.

Equilibrium relationships of mean wall stress [(Piri − Poro/(ro − ri)] and inside radius at five levels of distending pressure (6–60 mmHg). Passive elastic behavior of dilated arteriole (inset) is seen as solid squares. Hypothetical elastic diagram (open circles) assumes maintained shortening of vascular smooth muscle. Actual effects of reduction in pressure and hence stress in constricted vessel is seen in inset and is represented by line linking inverted triangles.

Data in inset redrawn from Gore 108
Figure 17. Figure 17.

Maximum decrease in mean diameter [(Do − Di)/2] as percentage of control (elicited by 250 nA · s dose of norepinephrine) expressed as function of initial tangential stress.

From Gore 108
Figure 18. Figure 18.

Relationship of constrictor responses (percent of maximum) of capacitance vessels (continuous line) and resistance vessels (broken line) to stimulation frequency in isolated hindquarters of a cat. Calculated fluid influx shown as fine broken line.

From Mellander 195
Figure 19. Figure 19.

Simplistic model of capacitance system consisting of an adjustable reservoir (screw) representing venomotor tone and a spring representing total venous compliance.
Figure 20. Figure 20.

Graphic solution of two equations: 1) dependence of right atrial pressure on cardiac output (venous return curve, c and d), and 2) dependence of cardiac output on right atrial pressure (Starling cardiac function curve, a and b). Point of intersection of a and c (t), which in an intact animal occurs at a right atrial pressure of about 0 mmHg, represents the stable operating point for the cardiovascular system at rest. Curve b represents an increased myocardial contractility, and curve d shows a decreased resistance to venous return. At zero cardiac output, pressure within all parts of circulation is same and is defined as mean circulatory filling pressure (mcfp).

Adapted from Guyton et al. 133
Figure 21. Figure 21.

Effect of prevailing venous pressure on magnitude of total active and passive blood mobilization following vasoconstrictor nerve stimulation of isolated cat hindquarters preparation. At low pressures of about 2 mmHg, active and passive contributions are equal, whereas at higher pressures active emptying predominates.

From Öberg 211
Figure 22. Figure 22.

Hypothetical relationship of volume to pressure within one or more veins before active venoconstriction (curve I) and after active venoconstriction (curve II), in which no change in compliance occurred within observed pressure range of P1−P2. Change in compliance accompanying venoconstriction is represented by curve III. A loss of volume equal to ΔV1 + ΔV2 is partly compensated by active venoconstriction (ΔV1), but results in fall in pressure to P2 along curve II if no change in compliance occurs, or to P4 if compliance is decreased. Effects of fall in venous pressure is to mobilize passively volume ΔV1. In addition, venoconstriction with no changes in compliance adds further volume ΔV2 to total. If compliance is reduced, however, as seen in curve III, additional volume (ΔV3) mobilized is less than that given by curve II.
Figure 23. Figure 23.

Electrical analogue characterizing relationship of pressure changes and total capacity of systemic circulatio.

From Shoukas and Sagawa 262, by permission of the American Heart Association, Inc
Figure 24. Figure 24.

Time dependence of total systemic vascular compliance. P values indicate statistical significance of the difference in compliances between intact and vagotomized dogs. Triangles indicate lumped data for intact and vagotomized dogs.

From Shoukas and Sagawa 262, by permission of the American Heart Association, Inc
Figure 25. Figure 25.

Mean pressure‐volume relationships (“effective” compliance) calculated from data obtained from 8 subjects by measuring changes in central venous pressure resulting from infusion and removal of dextran/blood. Because all recorded relationships showed hysteresis, above points at each value of volume were obtained as mean of two volumes at corresponding pressure values, one on ascending limb, the other on descending limb. NE and LBPP denote norepinephrine and lower body positive pressure, the latter produced by enclosing lower half of subject in a box up to level of xiphoideus sterni.

From Echt et al. 81, by permission of the American Heart Association, Inc
Figure 26. Figure 26.

Simple series‐coupled resistive and capacitative models of circulation.

two‐reservoir model after Guyton et al. 133.

two‐reservoir model of Berne and Levy 37.

3‐reservoir model.
Figure 27. Figure 27.

Parallel reservoir model of circulation. C1 and C2, compliances; , and , arterial resistances; and , venous resistances; Pra, right atrial pressure.

From Caldini et al. 51, by permission of the American Heart Association, Inc
Figure 28. Figure 28.

Semilog plot of ratio of blood volume (Vt − Vss) still to change at time t, to total volume change between two steady states V1 and Vss as function of time following step decrease in right atrial pressure while maintaining constant flow.

From Caldini et al. 51, by permission of the American Heart Association, Inc
Figure 29. Figure 29.

Relationships of flow () and right atrial pressure (Pra) before and during epinephrine infusion calculated for isovolumic conditions. Broken line represents effect of epinephrine on elastic and resistive properties alone.

From Caldini et al. 51, by permission of the American Heart Association, Inc


Figure 1.

effect of section of lumbar sympathetic trunk at L3−L4 on outside diameter (D) of dog femoral artery.

effect of stimulation of the lumbar sympathetic trunk at a level of L3−L4 on the outside diameter of a dog femoral artery. Stimulus parameters: 4.2 V, 5 ms, at 15 Hz. [From Gerová and Gero 102, by permission of the American Heart Association, Inc.]



Figure 2.

Equilibrium between internal (Pi) and external (Po) pressures and mean wall tension (T), which would have to be applied to both halves of longitudinally split, hollow cylinder to hold halves together.



Figure 3.

Elastic moduli (E) of relaxed and constricted carotid artery as function of strain and pressure, derived by Dobrin and Rovick from pressure‐circumference curves. At any pressure, E (constricted) < E (relaxed). “Unstressed” circumference of constricted vessel was used to compute strain for both constricted and relaxed vessels, leading to erroneous conclusion that at comparable strain, constricted vessels have lower elastic moduli. Compare this to same data plotted in Fig. 4 using appropriate “unstressed” circumferences to compute strain.

From Dobrin and Rovick 76


Figure 4.

Stress‐strain relationships of relaxed and constricted carotid artery derived from data of Dobrin and Rovick 76. Strain was calculated for each by using appropriate “unstressed” circumferences obtained at pressures of approximately 5 mmHg. At most strain and stress values and at comparable distending pressures, slope of stress‐strain curve is lower, that is, elastic modulus is lower for constricted vessel.



Figure 5.

Dependence of dynamic elastic modulus on arterial pressure. DTA, descending thoracic aorta; ABA, abdominal aorta; BCA, brachiocephelic artery; LSC, left subclavian artery; CA, carotid artery; FA, femoral artery. Note relatively greater pressure dependence of elasticity in peripheral arteries.

From Cox 64


Figure 6.

Pressure‐radius relationships for rabbit ear artery, showing little change in ΔP/Δro within normal range of arterial pressure despite very different degrees of vascular smooth muscle contraction. Curves are fully constricted (closed circles), intermediately constricted (closed squares), and fully relaxed (open and closed triangles). Epinephrine and a 60‐min period of electrical stimulation at 4 Hz were used to produce full or partial constriction. Open circles show response of artery to increasing pressure after electrical stimulation but without added epinephrine.



Figure 7.

Vascular input impedance (modulus and phase) of systemic circulation of dog plotted against frequency. Note relatively stable impedance modulus at frequencies above that of resting heart rate (2 Hz). This should be compared to higher values between 0 and 2 Hz and modulus of input impedance of simple elastic tube terminated by hydraulic resistance (Fig. 8 A). (Coherence is a measure of association between the variables and is akin to a correlation coefficient.

From Taylor 278, by permission of the American Heart Association, Inc


Figure 8.

Top: input impedance of branching assembly of elastic tubes (solid line) compared with that of single “equivalent” tube (broken line). Reflection coefficient is 0.6 in both cases, so that |Z0|0 at zero frequency is 11.5. Note reduction of modulus spikes, hence a greater stability of |Z0|0 when multiple tubes are present in model. Bottom: input impedance of random‐length, branching assembly as in Top, showing stabilizing effects on both modulus and phase of viscous properties (largely of smooth muscle) of vessel walls. Solid line shows no viscosity, dashed line represents phase angle of 10° for viscoelastic modulus, and dotted line shows phase angle of 20°. Results of wall viscosity are similar to fluid viscosity, except that latter elevates impedance modulus at zero frequency (i.e., input resistance).

From Taylor 277


Figure 9.

Mean systemic input impedance modulus and phase for 12 unanesthetized dogs before (open circles) and following (closed circles) carotid sinus hypotension produced by occlusion of brachiocephalic artery. Note increase in characteristic impedance, part of which may be due to elevated systemic pressure and its effect on elasticity, and part due to reduction cross‐sectional area of arterial tree.

From Cox et al. 67


Figure 10.

Effect of elevated blood pressure induced by norepinephrine injection on systemic vascular input impedance. Note shift to right of minima of modulus from roughly 3 and 8 Hz to 5 and 10 Hz, respectively. Failure of characteristic impedance to rise suggests that pressure‐induced increases in elasticity of arterial tree were offset by increases in its cross‐sectional area.

From O'Rourke and Taylor 219, by permission of the American Heart Association, Inc


Figure 11.

Vascular impedance of dog femoral artery showing effects of vasodilatation on modulus and phase. Reduction in reflection coefficient flattens undulations in modulus and phase. Shift to left of impedance modulus minimum is not completely explained by the random tube model 277,218, but such a disparity might be expected to arise from geometric dissimilarities between model and femoral vascular bed. Intercept of phase on frequency axis was variable—intercept during dilatation occurred at lower frequencies and supported model 277,218, whereas in later study 218 it occurred at a higher frequency than the control.

From Taylor 278, by permission of the American Heart Association, Inc


Figure 12.

Changes in contour and timing of peaks of simultaneously recorded femoral pressure waves and flow waves following vasodilatation induced by close arterial injection of acetylcholine. Note close correspondence of pressure and flow during dilatation, which can be anticipated when reflections are substantially reduced. Mean blood pressure: 107 mmHg (control), 94 mmHg (vasodilated). Mean flow: 1.08 ml/s (control), 6.93 ml/s (vasodilated).

From O'Rourke and Taylor 218, by permission of the American Heart Association, Inc


Figure 13.

Modulus of vascular impedance of systemic circulation and impedance of renal, celiac, and femoral vascular beds under control conditions (open circles), reflex constriction (solid squares), and reflex dilatation (solid triangles) before and after bilateral vagotomy. In renal and celiac beds, vasoconstriction elevated impedance and vasodilatation reduced impedance at all frequencies, although this was true only for first four harmonies in femoral bed.

From Cox and Bagshaw 66, by permission of the American Heart Association, Inc


Figure 14.

Changes in relative contribution of oscillatory power to total cardiac power (oscillatory power fraction) as function of heart frequency, and influence on control relationship (open circles) of isoproterenol (uppermost curve, open squares), norepinephrine (solid circles), and angiotensin (lowest curve, closed squares). Isoproterenol elevated cardiac output and total cardiac power but increased pulsatile losses, thereby reducing cardiac efficiency.

From Cox 62


Figure 15.

Profile of pressure drops through systemic circulation, demonstrating major site of vascular resistance in precapillary vessels and showing increase and decrease in capillary pressure, which occurs during precapillary vasodilatation and vasoconstriction, respectively.

From Keele and Neil 163


Figure 16.

Equilibrium relationships of mean wall stress [(Piri − Poro/(ro − ri)] and inside radius at five levels of distending pressure (6–60 mmHg). Passive elastic behavior of dilated arteriole (inset) is seen as solid squares. Hypothetical elastic diagram (open circles) assumes maintained shortening of vascular smooth muscle. Actual effects of reduction in pressure and hence stress in constricted vessel is seen in inset and is represented by line linking inverted triangles.

Data in inset redrawn from Gore 108


Figure 17.

Maximum decrease in mean diameter [(Do − Di)/2] as percentage of control (elicited by 250 nA · s dose of norepinephrine) expressed as function of initial tangential stress.

From Gore 108


Figure 18.

Relationship of constrictor responses (percent of maximum) of capacitance vessels (continuous line) and resistance vessels (broken line) to stimulation frequency in isolated hindquarters of a cat. Calculated fluid influx shown as fine broken line.

From Mellander 195


Figure 19.

Simplistic model of capacitance system consisting of an adjustable reservoir (screw) representing venomotor tone and a spring representing total venous compliance.



Figure 20.

Graphic solution of two equations: 1) dependence of right atrial pressure on cardiac output (venous return curve, c and d), and 2) dependence of cardiac output on right atrial pressure (Starling cardiac function curve, a and b). Point of intersection of a and c (t), which in an intact animal occurs at a right atrial pressure of about 0 mmHg, represents the stable operating point for the cardiovascular system at rest. Curve b represents an increased myocardial contractility, and curve d shows a decreased resistance to venous return. At zero cardiac output, pressure within all parts of circulation is same and is defined as mean circulatory filling pressure (mcfp).

Adapted from Guyton et al. 133


Figure 21.

Effect of prevailing venous pressure on magnitude of total active and passive blood mobilization following vasoconstrictor nerve stimulation of isolated cat hindquarters preparation. At low pressures of about 2 mmHg, active and passive contributions are equal, whereas at higher pressures active emptying predominates.

From Öberg 211


Figure 22.

Hypothetical relationship of volume to pressure within one or more veins before active venoconstriction (curve I) and after active venoconstriction (curve II), in which no change in compliance occurred within observed pressure range of P1−P2. Change in compliance accompanying venoconstriction is represented by curve III. A loss of volume equal to ΔV1 + ΔV2 is partly compensated by active venoconstriction (ΔV1), but results in fall in pressure to P2 along curve II if no change in compliance occurs, or to P4 if compliance is decreased. Effects of fall in venous pressure is to mobilize passively volume ΔV1. In addition, venoconstriction with no changes in compliance adds further volume ΔV2 to total. If compliance is reduced, however, as seen in curve III, additional volume (ΔV3) mobilized is less than that given by curve II.



Figure 23.

Electrical analogue characterizing relationship of pressure changes and total capacity of systemic circulatio.

From Shoukas and Sagawa 262, by permission of the American Heart Association, Inc


Figure 24.

Time dependence of total systemic vascular compliance. P values indicate statistical significance of the difference in compliances between intact and vagotomized dogs. Triangles indicate lumped data for intact and vagotomized dogs.

From Shoukas and Sagawa 262, by permission of the American Heart Association, Inc


Figure 25.

Mean pressure‐volume relationships (“effective” compliance) calculated from data obtained from 8 subjects by measuring changes in central venous pressure resulting from infusion and removal of dextran/blood. Because all recorded relationships showed hysteresis, above points at each value of volume were obtained as mean of two volumes at corresponding pressure values, one on ascending limb, the other on descending limb. NE and LBPP denote norepinephrine and lower body positive pressure, the latter produced by enclosing lower half of subject in a box up to level of xiphoideus sterni.

From Echt et al. 81, by permission of the American Heart Association, Inc


Figure 26.

Simple series‐coupled resistive and capacitative models of circulation.

two‐reservoir model after Guyton et al. 133.

two‐reservoir model of Berne and Levy 37.

3‐reservoir model.



Figure 27.

Parallel reservoir model of circulation. C1 and C2, compliances; , and , arterial resistances; and , venous resistances; Pra, right atrial pressure.

From Caldini et al. 51, by permission of the American Heart Association, Inc


Figure 28.

Semilog plot of ratio of blood volume (Vt − Vss) still to change at time t, to total volume change between two steady states V1 and Vss as function of time following step decrease in right atrial pressure while maintaining constant flow.

From Caldini et al. 51, by permission of the American Heart Association, Inc


Figure 29.

Relationships of flow () and right atrial pressure (Pra) before and during epinephrine infusion calculated for isovolumic conditions. Broken line represents effect of epinephrine on elastic and resistive properties alone.

From Caldini et al. 51, by permission of the American Heart Association, Inc
References
 1. Aars, H. Effects of altered smooth muscle tone on aortic diameter and aortic baroreceptor activity in anesthetised rabbits. Circulation Res. 28: 254–262, 1971.
 2. Abdel‐Sayed, W. A., F. M. Abboud, and D. R. Ballard. Contribution of venous resistance to total vascular resistance in skeletal muscle. Am. J. Physiol. 218: 1291–1295, 1970.
 3. Abel, F. L. Fourier analysis of left ventricular performance. Evaluation of impedance matching. Circulation Res. 28: 119–135, 1968.
 4. Alexander, R. S. The participation of the venomotor system in pressor reflexes. Circulation Res. 2: 405–409, 1954.
 5. Alexander, R. S. The peripheral venous system. In: Handbook of Physiology. Circulation, edited by W. F. Hamilton. Washington, DC: Am. Physiol. Soc., 1963, sect. 2, vol. II, chapt. 31, p. 1075–1093.
 6. Alexander, R. S. Critical closure reexamined. Circulation Res. 40: 531–535, 1977.
 7. Apéria, A. Haemodynamical studies. Skand. Arch. Physiol. 83: (Suppl.) 1–230, 1940.
 8. Arndt, J. O., H. F. Stegall, and H. J. Wicke. Mechanics of the aorta in vivo. A radiographic approach. Circulation Res. 28: 693–704, 1971.
 9. Astrand, P., and B. Saltin. Plasma and red cell volume after prolonged severe exercise. J. Appl. Physiol. 19: 829–832, 1964.
 10. Attinger, E. O. Elements of theoretical hydrodynamics. In: Pulsatile Blood Flow. edited by E. O. Attinger. New York: McGraw‐Hill, 1964, p. 15–76.
 11. Attinger, E. O. Wall properties of veins. IEEE Trans. Biomed. Eng. 16: 253–261, 1969.
 12. Attinger, E. O., and F. M. Attinger. Frequency dynamics of peripheral blood flow. In: Annual Reviews of Biophysics and Bioengineering, edited by L. J. Mullins et al. Palo Alto, CA: Ann. Rev., 1973, vol. 4, p. 7–36.
 13. Attinger, F. M. L. Two dimensional in vitro studies of femoral arterial walls of the dog. Circulation Res. 22: 829–840, 1968.
 14. Avolio, A. P., M. F. O'Rourke, K. Mang, P. T. Bason, and B. S. Gow. A comparative study of pulsatile arterial hemodynamics in rabbits and guinea pigs. Am. J. Physiol. 230: 868–875, 1976.
 15. Ayers, A. B., B. N. Davies, and P. G. Witherington. Responses of the isolated perfused human spleen to sympathetic nerve stimulation, catecholamines and polypeptides. Brit. J. Pharmacol. 44: 17–30, 1972.
 16. Azuma, T., and S. Oka. Mechanical equilibrium of blood vessel walls. Am. J. Physiol. 221: 1310–1318, 1971.
 17. Bader, H. The anatomy and physiology of the vascular wall. In: Handbook of Physiology. Circulation, edited by W. F. Hamilton. Washington, DC: Am. Physiol. Soc., 1963, sect. 2, vol. II, chapt. 26, p. 865–889.
 18. Baeckström, P., B. Folkow, E. Kendrick, B. Lofving, and B. Öberg. Effects of vasoconstriction on blood viscosity in vivo. Acta Physiol. Scand. 81: 376–384, 1971.
 19. Baez, S., and H. Lamport. On the nature of the unchanging diameter in isolated microscopic vessels under pressure variation. Physiologist 3: 13, 1960. [Cited by Green et al. (122).]
 20. Bagshaw, R. J., and L. H. Peterson. Sympathetic control of the mechanical properties of the canine carotid sinus. Am. J. Physiol. 222: 1462–1468, 1972.
 21. Barcroft, H., and A. Samaan. Explanation of the increase in systemic flow caused by occluding the descending thoracic aorta. J. Physiol. London 85: 47–61, 1935.
 22. Barcroft, J., H. A. Harris, D. Orahovarts, and R. Weiss. A contribution to the physiology of the spleen. J. Physiol. London 60: 443–456, 1925.
 23. Barcroft, J., Y. Nisimaru, and S. R. Puri. The action of the splanchnic nerves on the spleen. J. Physiol. London 74: 321–326, 1932.
 24. Barcroft, J., and J. G. Stephens. Observations upon the size of the spleen. J. Physiol. London 64: 1–22, 1927.
 25. Bargainer, J. D. Puke wave velocity in the main pulmonary artery of the dog. Circulation Res. 20: 630–637, 1967.
 26. Barnett, G. O., A. J. Mallos, and A. Shapiro. Relationship of aortic pressure and diameter in the dog. J. Appl. Physiol. 16: 545–548, 1961.
 27. Bartelstone, H. J. Role of the veins in venous return. Circulation Res. 8: 1059–1076, 1960.
 28. Bauer, R. D., and R. Busse (editors). The Arterial System. Berlin: Springer, 1978.
 29. Baum, T., and M. J. Hosko, Jr. Response of resistance and capacitance vessels to central nervous system stimulation. Am. J. Physiol. 209: 236–242, 1965.
 30. Bayliss, L. E. The rheology of blood. In: Handbook of Physiology, edited by W. F. Hamilton. Washington, DC: Am. Physiol. Soc., 1962, sect. 2, vol. I, chapt. 8, p. 137–150.
 31. Bayliss, W. M. On the reactions of the arterial wall to changes in internal pressure. J. Physiol. London 28: 220–231, 1902.
 32. Benninghoff, A. Über die Beziehungen zwischen elastichen Gerüst und glatter Muskulatur in der Arterienwand und ihre functionelle Bedeutung. Z. Zellforsch. Mikroskop. Anat. 6: 348–396, 1928.
 33. Bergel, D. H. The dynamic elastic properties of the arterial wall. J. Physiol. London 156: 458–469, 1961.
 34. Bergel, D. H. The static elastic properties of the arterial wall. J. Physiol. London 156: 445–457, 1961.
 35. Bergel, D. H., and W. R. Milnor. Pulmonary vascular impedance in the dog. Circulation Res. 16: 401–415, 1965.
 36. Bergel, D. H. The measurement of lengths and dimensions. In: Cardiovascular Fluid Dynamics, edited by D. H. Bergel. New York: Academic, 1972, vol. I, p. 91–114.
 37. Bergström, J., G. Guarnieri, and E. Hultman. Carbohydrate metabolism and electrolyte changes in human muscle tissue during heavy work. J. Appl. Physiol. 30: 122–125, 1971.
 38. Berne, R. M., and M. N. Levy. Cardiovascular Physiology. St. Louis: Mosby, 1977, p. 196.
 39. Blakeley, A. G. H. The responses of the spleen to nerve stimulation in relation to the frequency of splenic nerve discharge. Proc. Roy. Soc. London Ser. B. 171: 201–211, 1968.
 40. Blick, E. F., and P. D. Stein. A review of second order effects on Poiseuille's equation for application to blood and other viscous fluids. Med. Res. Eng. 11: 26–31, 1976.
 41. Boatman, D. L., and M. J. Brody. Analysis of vascular responses in the spleen. Am. J. Physiol. 207: 155–161, 1964.
 42. Bramwell, J. C., and A. V. Hill. The velocity of the pulse wave in man. Proc. Roy. Soc. London Ser. B. 93: 298–306, 1922.
 43. Brender, D., and M. M. Webb‐Pebloe. Influence of carotid baroreceptors on different components of the vascular system. J. Physiol. London 205: 257–274, 1969.
 44. Brooksby, G. A., and D. E. Donald. Dynamic changes in splanchnic bloodflow and blood volume in dogs during activation of sympathetic nerves. Circulation Res. 29: 227–238, 1971.
 45. Brooksby, G. A., and D. E. Donald. Release of blood from the splanchnic circulation in dogs. Circulation Res. 31: 105–118, 1972.
 46. Browse, N. L., D. E. Donald, and J. T. Shepherd. Role of the veins in the carotid sinus reflex. Am. J. Physiol. 210: 1424–1434, 1966.
 47. Browse, N. L., R. R. Lorenz, and J. T. Shepherd. Response of capacity and resistance vessels of dog's limb to sympathetic nerve stimulation. Am. J. Physiol. 210: 95–102, 1966.
 48. Burton, A. C. On the physical equilibrium of small blood vessels. Am. J. Physiol. 164: 319–329, 1951.
 49. Burton, A. C. Relation of structure to function of the tissues of the wall of blood vessels. Physiol. Rev. 34: 619–642, 1954.
 50. Burton, A. C. Physiology and Biophysics of the Circulation. Chicago: Year Book Med. 1965, p. 63.
 51. Burton‐Opitz, R. Über die Strömung des Blutes in dem Gebiete der Pfortader II. Das Strömvolum de Vena lienalis. Pfluegers Arch. Ges. Physiol. 129: 189–216, 1909.
 52. Caldini, P., S. Permutt, J. A. Waddell, and R. L. Riley. Effect of epinephrine on pressure, flow, and volume relationships in the systemic circulation of dogs. Circulation Res. 34: 606–623, 1974.
 53. Carew, T. E., R. N. Vaishnav, and D. J. Patel. Compressibility of the arterial wall. Circulation Res. 23: 61–68, 1968.
 54. Carniero, J. J., and D. E. Donald. Change in liver blood flow and blood content in dogs during direct and reflex stimulation of sympathetic nerve activity. Circulation Res. 40: 150–158, 1977.
 55. Caro, C. G., T. J. Pedley, R. C. Shroter, and W. A. Seed. The Mechanics of the Circulation. London: Oxford, 1978.
 56. Casson, N. A flow equation for pigment‐oil suspensions of the printing ink type. In: Rheology of Disperse Systems, edited by C. C. Mills. Oxford: Pergamon, 1959, p. 84–104.
 57. Charm, S. E., and G. S. Kurland. Blood rheology. In: Cardiovascular Fluid Dynamics, edited by D. H. Bergel. New York: Academic, 1972, vol. II, p. 157–203.
 58. Celander, O. The range of control exercised by the sympathicoadrenal system. Acta Physiol. Scand. 32: (Suppl. 116) 1–132, 1954.
 59. Chien, S. Role of the sympathetic nervous system in hemorrhage. Physiol. Rev. 47: 214–288, 1967.
 60. Chien, S., and S. Usami. Relation of sympathetic system to the effects of haemorrhage on splanchnic circulation (Abstract). Federation. Proc. 21: 124, 1962.
 61. Coles, D. R. Heat elimination from the toes during exposure of the foot to subatmospheric pressures. J. Physiol. London 135: 171–181, 1957.
 62. Coles, D. R., and A. D. M. Greenfield. The reactions of blood vessels of the hand during increases in transmural pressures. J. Physiol. London 131: 277–289, 1956.
 63. Cox, R. H. Determinants of systemic hydraulic power in unanesthetized dogs. Am. J. Physiol. 226: 579–587, 1974.
 64. Cox, R. H. Anisotropic properties of the canine carotid artery in vitro. J. Biomech. 8: 293–300, 1975.
 65. Cox, R. H. Pressure dependence of the mechanical properties of arteries in vivo. Am. J. Physiol. 229: 1371–1375, 1975.
 66. Cox, R. H. Mechanics of canine iliac artery smooth muscle in vitro. Am. J. Physiol. 230: 462–470, 1976.
 67. Cox, R. H., and R. J. Bagshaw. Baroreceptor reflex control of arterial haemodynamics in the dog. Circulation Res. 37: 772–786, 1975.
 68. Cox, R. H., A. Fronek, and L. H. Peterson. Effects of carotid hypotension on aortic hemodynamics in the unanesthetized dog. Am. J. Physiol. 229: 1376–1380, 1975.
 69. Cumming, G. The pulmonary circulation. In: Cardiovascular Physiology I, edited by A. C. Guyton and C. E. Jones. London: Butterworths, 1974, vol. 1, p. 93–122. (Intern. Rev. Physiol. Ser.)
 70. Daly, I. de B., H. N. Duke, C. O. Hebb, and J. Weatherall. Pulmonary vasomotor fibers in the sympathetic chain and its associated ganglia in the dog. Quart. J. Exptl. Physiol. 34: 285–313, 1948.
 71. Daly, I. de B., H. N. Duke, J. K. Linzell, and J. Weatherall. Pulmonary vasomotor nerve activity. Quart. J. Exptl. Physiol. 37: 149–162, 1952.
 72. Davies, B. N., B. H. Robinson, and P. G. Witherington. The effects of graded doses of phenoxybenzamine on the vascular and capsular responses of the isolated blood perfused dog spleen to sympathetic nerve stimulation and catecholamines. Arch. Intern. Pharmacodyn. 180: 143–154, 1969.
 73. Davies, B. N., and P. G. Witherington. The actions of drugs on the smooth muscle of the capsule and blood vessels of the spleen. Pharmacol. Rev. 25: 373–413, 1973.
 74. Davis, D. L. Effect of sympathetic stimulation on dog paw volume. Am. J. Physiol. 205: 989–994, 1963.
 75. Davson, H., and M. G. Eggleton. Principles of Human Physiology. London: Churchill, 1968, 14th ed.
 76. Djojosugito, A. M., B. Folkow, B. Öberg, and S. White. A comparison of blood viscosity measured in vitro and in a vascular bed. Acta Physiol. Scand. 78: 70–84, 1970.
 77. Dobrin, P. B., and J. M. Doyle. Vascular smooth muscle and the anisotropy of dog carotid artery. Circulation Res. 27: 105–119, 1970.
 78. Dobrin, P. B., and A. A. Rovick. Influence of vascular smooth muscle on contractile mechanics and elasticity of arteries. Am. J. Physiol. 217: 1644–1651, 1969.
 79. Donegan, J. F. The physiology of the veins. J. Physiol. London 55: 226–245, 1921.
 80. Drees, J. A., and C. F. Rothe. Reflex venoconstriction and capacity vessel pressure‐volume relationships in dogs. Circulation Res. 34: 360–373, 1974.
 81. Dresel, P., and I. Wallentin. Effects of sympathetic vasoconstrictor fibres, noradrenaline and vasopressin on the intestinal vascular resistance during constant blood flow or blood pressure. Acta Physiol. Scand. 66: 427–436, 1966.
 82. Ebert, R. V., and E. A. Stead. Demonstration that in normal man no reserves of blood are mobilised by exercise, epinephrine and haemorrhage. Am. J. Med. Sci. 201: 655–823, 1970.
 83. Echt, M., J. Düweling, O. H. Gauer, and L. Lange. Effective compliance of the total vascular bed and the intrathoracic compartment derived from changes in central venous pressure induced by volume changes in man. Circulation Res. 34: 61–68, 1974.
 84. Eliassen, E., B. Folkow, S. M. Hilton, B. Öberg, and B. Rippe. Pressure‐volume characteristics of the interstitial fluid space in the skeletal muscle of the cat. Acta Physiol. Scand. 90: 583–593, 1974.
 85. Elkins, R. C., and W. R. Milnor. Pulmonary vascular response to exercise in the dog. Circulation Res. 29: 591–599, 1971.
 86. Engelberg, J., and A. B. DuBois. Mechanics of pulmonary circulation in isolated rabbit lungs. Am. J. Physiol. 196: 401–414, 1959.
 87. Epstein, S. E., G. D. Beiser, M. Stampher, and E. Braunwald. Role of the venous system in baroreceptor‐mediated reflexes in man. J. Clin. Invest. 47: 139–152, 1968.
 88. Fischer, H. Uber die funktionelle Bedeutung des Spiralverlaufes der Muskulatur in der Arterienwand. Morphol. Jahrb. 91: 394–446, 1951.
 89. Folkow, B. A critical study of some methods used in investigations on the blood circulation. Acta Physiol. Scand. 27: 118–129, 1952.
 90. Folkow, B. Transmural pressure and vascular tone—some aspects of an old controversy. Arch. Intern. Pharmacodyn. 139: 455–469, 1962.
 91. Folkow, B. Description of the myogenic hypothesis. Circulation Res. 15: (Suppl. 1) 279–287, 1964.
 92. Folkow, B., D. H. Lewis, O. Lundren, S. Mellander, and I. Wallentin. The effect of graded vasoconstrictor fibre stimulation on the intestinal resistance and capacitance vessels. Acta Physiol. Scand. 61: 445–457, 1964.
 93. Folkow, B., and S. Mellander. Veins and venous tone. Am. Heart J. 68: 397–408, 1964.
 94. Folkow, B., and E. Neil. Circulation. New York: Oxford, 1971.
 95. Francois‐Frank, C. A., and L. Hallion. Recherches experimentales sur l'innervation vaso‐constrictive du foie. Arch. Physiol. Norm. Pathol. 8: 908–922, 1896.
 96. Frank, O. Die Grundform des Arteriellen Pulses. Erste Abhandlung. Mathematische Analyse. Z. Biol. 37: 483–526, 1899.
 97. Franklin, K. J. A Monograph on Veins. Springfield, Ill.: Thomas, 1937.
 98. Fung, Y‐C. B. Biomechanics: its scope, history and some problems of continuum mechanics in physiology. Appl. Mech. Rev. 21: 1–20, 1968.
 99. Fuxe, K., and G. Sedvall. The distribution of adrenergic nerve fibres to the blood vessels in skeletal muscle. Acta Physiol. Scand. 64: 75–86, 1965.
 100. Gaffney, T. E., W. M. Bryant, and E. Braunwald. Effects of reserpine and guanethidine on venous reflexes. Circulation Res. 11: 889–894, 1962.
 101. Gauer, O. H., and J. P. Henry. Neurohormonal control of plasma volume. In: Cardiovascular Physiology II, edited by A. C. Guyton and A. W. Cowley. Baltimore: Univ. Park, 1976, vol. 9. (Intern. Rev. Physiol. Ser.)
 102. Gauer, O. H., and H. L. Thron. Properties of veins in vivo: integrated effects of their smooth muscle. Physiol. Rev. 42: 283–303, 1962.
 103. Gauer, O. H., and H. L. Thron. Postural changes in the circulation. In: Handbook of Physiology. Circulation, edited by W. F. Hamilton. Washington, DC: Am. Physiol. Soc., 1965, sect. 2, vol. III, chapt. 67, p. 2409–2440.
 104. Gero, J., and M. Gerová. Sympathetic regulation of arterial distensibility. Physiol. Bohemoslov. 18: 480–481, 1969.
 105. Gerová, M., and J. Gero. Range of the sympathetic control of the dog femoral artery. Circulation Res. 24: 349–359, 1969.
 106. Gerová, M., J. Gero, S. Doležel, and I. Blažková‐Huzuláková. Sympathetic control of canine abdominal aorta. Circulation Res. 33: 149–159, 1973.
 107. Gessner, U. Vascular input impedance. In: Cardiovascular Fluid Dynamics, edited by D. H. Bergel. New York: Academic, 1972, vol. I, p. 315–349.
 108. Goltz, F. Ueber den tonus de Gefässe und seine Bedeutung für die Blutbewegung. Arch. Pathol. Anat Physiol. 29: 394–432, 1864.
 109. Gore, R. W. Wall stress: a determinant of regional differences in response of frog microvessels to norepinephrine. Am. J. Physiol. 222: 82–91, 1972.
 110. Gore, R. W. Pressures in cat mesenteric arterioles and capillaries during changes in systemic arterial blood pressure. Circulation Res. 34: 581–591, 1974.
 111. Gosling, R. G., and D. H. King. Continuous wave ultrasound as an alternative and complement to Xrays in vascular examinations. In: Cardiovascular Applications of Ultrasound, edited by R. S. Reneman. New York: Elsevier, 1974, p. 265–282.
 112. Gow, B. S. An electrical caliper for measurement of pulsatile arterial diameter changes in vivo. J. Appl. Physiol. 21: 1122–1126, 1966.
 113. Gow, B. S. Viscoelastic properties of conduit arteries. Circulation Res. 26, (Suppl. 2) 113–122, 1970.
 114. Gow, B. S. The influence of vascular smooth muscle on the viscoelastic properties of blood vessels. In: Cardiovascular Fluid Dynamics, edited by D. H. Bergel, New York: Academic, 1972, vol. II, p. 65–110.
 115. Gow, B. S., and C. Hadfield. The elastic properties of human and canine epicardial coronary arteries. Circulation Res. 45: 588–594, 1979.
 116. Gow, B. S., D. Schonfeld, and D. J. Patel. The dynamic elastic properties of the canine left circumflex coronary artery. J. Biomech. 7: 389–395, 1974.
 117. Gow, B. S., and M. G. Taylor. Measurement of viscoelastic properties of arteries in the living dog. Circulation Res. 23: 111–122, 1968.
 118. Grayson, J., and D. Mendel. Physiology of the Splanchnic Circulation. London: Arnold, 1965 (Monographs of the Physiological Society.)
 119. Green, H. D., C. E. Rapela, and M. C. Conrad. Resistance (conductance) and capacitance phenomena in terminal vascular beds. In: Handbook of Physiology. Circulation, edited by W. F. Hamilton. Washington, DC: Am. Physiol. Soc., 1965, sect. 2, vol. II, chapt. 28, p. 935–960.
 120. Greenfield, A. D. M., and G. C. Patterson. Reactions of the blood vessels of the human forearm to increases in transmural pressure. J. Physiol. London 125: 508–524, 1954.
 121. Greenway, C. V., A. E. Lawson, and S. Mellander. The effects of stimulation of the hepatic nerves, infusions of noradrenaline and occlusion of the carotid arteries on liver blood flow in the anaesthetised cat. J. Physiol. London 192: 21–41, 1967.
 122. Greenway, C. V., A. E. Lawson, and R. D. Stark. Vascular responses of the spleen to nerve stimulation during normal and reduced blood flow. J. Physiol. London 194: 421–433, 1968.
 123. Greenway, C. V., and G. E. Lister. Capacitance effects and blood reservoir function in the splanchnic vascular bed during non‐hypotensive haemorrhage and blood volume expansion in anaesthetised cats. J. Physiol. London 237: 279–294, 1974.
 124. Greenway, C. V., and G. Oshiro. Comparison of the effects of hepatic nerve stimulation on arterial flow, distribution of arterial and portal flows and blood content in the livers of anaesthetised cats and dogs. J. Physiol. London 227: 487–501, 1972.
 125. Greenway, C. V., and R. D. Stark. Vascular responses of the spleen to rapid haemorrhage in the anaesthetised cat. J. Physiol. London 204: 169–179, 1969.
 126. Greenway, C. V., and R. D. Stark. Hepatic vascular bed. Physiol. Rev. 51: 23–65, 1971.
 127. Greenway, C. V., R. D. Stark, and W. W. Lautt. Capacitance responses and fluid exchange in the cat liver during stimulation of the hepatic nerves. Circulation Res. 25: 277–284, 1969.
 128. Grega, G. J., J. M. Schwinghamer, and F. J. Haddy. Changes in forelimb weight and segmental resistances following severe haemorrhages. Circulation Res. 29: 691–703, 1971.
 129. Greenwald, S. E., D. L. Newman, and N. L. R. Bowden. Comparison between theoretical and directly measured pulse propagation velocities in the aorta of the anaesthetized dog. Cardiovascular Res. 12: 407–414, 1978.
 130. Griffith, F. R., Jr., and F. E. Emery. The vasomotor control of the liver circulation. Am. J. Physiol. 95: 20–34, 1930.
 131. Groom, A. C., S. Rowlands, and H. W. Thomas. Some circulatory responses to haemorrhage in the cat; a critical level of blood volume for the onset of hypotension. Quart. J. Exptl. Physiol. 211: 712–720, 1965.
 132. Groom, A. C., S. Rowlands, and H. W. Thomas. Some circulatory responses to haemorrhage in the cat. Quart. J. Exptl. Physiol. 50: 385–405, 1965.
 133. Guntheroth, W. G. In vivo measurement of dimensions of veins with implications regarding control of venous return. IEEE Trans. Biomed. Eng. 16: 247–253, 1969.
 134. Guntheroth, W. G., and G. L. Mullins. Liver and spleen as venous reservoirs. Am. J. Physiol. 204: 35–41, 1963.
 135. Guyton, A. C., G. G. Armstrong, and P. L. Chipley. Pressure‐volume curves of the arterial and venous systems in live dogs. Am. J. Physiol. 184: 253–258, 1956.
 136. Guyton, A. C., C. E. Jones, and T. G. Coleman. Circulatory Physiology: Cardiac Output and Its Regulation. Philadelphia: Saunders, 1973.
 137. Guyton, A. C., A. W. Lindsey, B. Abernathy, and J. B. Langston. Mechanism of the increased venous return and cardiac output caused by epinephrine. Am. J. Physiol. 192: 126–130, 1958.
 138. Guyton, A. C., A. W. Lindsey, and B. N. Kaufmann. Effect of mean circulatory filling pressure and other peripheral circulatory factors on cardiac output. Am. J. Physiol. 180: 463–468, 1955.
 139. Guyton, A. C., A. E. Taylor, and H. J. Granger. Circulatory Physiology II: Dynamics and Control of the Body Fluids. Philadelphia: Saunders, 1975.
 140. Haddy, F. J., J. I. Molnar, and R. W. Campbell. Effects of denervation and vasoactive agents on vascular pressures and weight of dog forelimb. Am. J. Physiol. 201: 631–638, 1961.
 141. Haddy, F. J., J. B. Scott, and G. J. Grega. Peripheral circulation: Fluid transfer across the microvascular membrane. In: Cardiovascular Physiology II, edited by A. C. Guyton and A. W. Cowley. Baltimore: Univ. Park, 1976, vol. 9, p. 63–109. (Intern. Rev. Physiol. Ser.)
 142. Haddy, F. J., J. B. Scott, and J. I. Molnar. Mechanism of volume replacement and vascular constriction following hemorrhage. Am. J. Physiol. 208: 169–181, 1965.
 143. Hadjimanas, J., and B. Öberg. Effects of carotid baroreceptor reflexes on venous tone in skeletal muscle and intestine of the cat. Acta Physiol. Scand. 72: 518–532, 1968.
 144. Hainsworth, R., and R. J. Linden. Reflex control of vascular capacitance. In: Cardiovascular Physiology III, edited by A. C. Guyton and D. B. Young. Baltimore: Univ. Park, 1978, vol. 18, p. 67–124. (Intern. Rev. Physiol. Ser.)
 145. Hales, S. Statik des Geblüts, Halle, 1748.
 146. Hardung, V. Propagation of pulse waves in visco‐elastic tubings. In: Handbook of Physiology. Circulation, edited by W. F. Hamilton. Washington, DC: Am. Physiol. Soc., 1962, sect. 2, vol. I, chapt. 7, p. 107–135.
 147. Hardung, V. Die Bedeutung der Anisotropie und Inhomogenität bei der Bestimmung der Elastizität der Blutgefässe II. Angiologica 1: 185–196, 1964.
 148. Harlan, J. C., E. E. Smith, and T. Q. Richardson. Pressure‐volume curves of systemic and pulmonary circuit. Am. J. Physiol. 213: 1499–1503, 1967.
 149. Hartley, L. H., B. Pernow, J. Häggendal, J. Lacour, J. de Lattre, and B. Saltin. Central circulation during sub‐maximal work preceded by heavy exercise. J. Appl. Physiol. 29: 818–823, 1970.
 150. Henry, J. P., and M. D. Meehan. The Circulation: An Integrative Physiologic Study. Chicago: Year Book Med., 1971.
 151. Herndon, C. W., and K. Sagawa. Combined effects of aortic and right atrial pressures on aortic flow. Am. J. Physiol. 217: 65–72, 1969.
 152. Heymans, C., and E. Neil. Reflexogenic Areas of the Cardiovascular System. London: Churchill, 1958.
 153. Hinke, J. A. In vitro demonstration of vascular hyper responsiveness in experimental hypertension. Circulation Res. 17: 359–371, 1965.
 154. Hochberger, A. I., and B. W. Zweifach. Analysis of critical closing pressure in the perfused rabbit ear. Am. J. Pathol. 214: 962–968, 1968.
 155. Hokanson, D. E., D. J. Mozersky, D. S. Sumner, and D. E. Strandness, Jr. A phase‐locked echo tracking system for recording arterial diameter changes in vivo. J. Appl. Physiol. 32: 728–733, 1972.
 156. Ingram, R. H., Jr., J. P. Szidon, and A. P. Fishman. Response of the main pulmonary artery of dogs to neurally released versus blood‐borne norepinephrine. Circulation Res. 26: 249–262, 1970.
 157. Ingram, R. H., Jr., J. P. Szidon, R. Skalak, and A. P. Fishman. Effects of sympathetic nerve stimulation on the pulmonary arterial tree of the isolated lobe perfused in situ. Circulation Res. 22: 801–815, 1968.
 158. Intaglietta, M. Pressure measurement in the microcirculation with active and passive transducers. Microvascular Res. 5: 317–323, 1975.
 159. Intaglietta, M., and B. W. Zweifach. Microcirculatory basis of fluid exchange. Advan. Biol. Med. Phys. 15: 111–159, 1974.
 160. Jacobsson, S., and I. Kjellmer. Accumulation of fluid in exercising skeletal muscle. Acta Physiol. Scand. 60: 286–292, 1964.
 161. Järhult, J. Osmolar control of the circulation in haemorrhagic hypotension. Acta. Physiol. Scand. Suppl. 423: 1–84, 1975.
 162. Johnson, P. C. Autoregulatory responses of cat mesenteric arterioles measured in vivo. Circulation Res. 22: 199–212, 1968.
 163. Johnson, P. C. The microcirculation and local and humoral control of the circulation. In: Cardiovascular Physiology I, edited by A. C. Guyton and C. E. Jones. London: Butterworths, 1974, vol. 1, p. 163–195. (Intern. Rev. Physiol. Ser.)
 164. Johnson, P. C., and E. E. Selkurt. Intestinal weight changes in hemorrhagic shock. Am. J. Physiol. 193: 135–143, 1958.
 165. Keatinge, W. R. Electrical and mechanical response of arteries to stimulation of sympathetic nerves. J. Physiol. London 185: 701–715, 1966.
 166. Keele, C. A., and E. Neil. Samson Wright's Applied Physiology. London: Oxford, 1971.
 167. Kezdi, P. Baroreceptors and Hypertension. Oxford: Pergamon, 1967.
 168. Kirchheim, H. R. Systemic arterial baroreceptor reflexes. Physiol. Rev. 56: 100–176, 1976.
 169. Kjellmer, I. The effect of exercise on the vascular bed of skeletal muscle. Acta. Physiol. Scand. 62: 18–30, 1964.
 170. Klemensiwicz, R. Cited by Gauer and Thron (101), p. 2429.
 171. Koizumi, K., and A. Sato. Influence of sympathetic innervation on carotid sinus baroreceptor activity. J. Physiol. London. 216: 321–329, 1969.
 172. Korner, P. I. Control of blood flow to special vascular areas: Brain, kidney, muscle, skin, liver and intestine. In: Cardiovascular Physiology I, edited by A. C. Guyton and C. E. Jones. London: Butterworths, 1974, vol. 1, p. 123–162. (Intern. Rev. Physiol. Ser.)
 173. Koubenec, H. J., and O. H. Gauer. Effective compliance of the total vascular system of man sitting and immersed in a bath. Pfluegers Arch. European J. Physiol. 355: (Suppl.) R24, 1975. [Cited by Gauer and Henry, (99).]
 174. Krafka, J., Jr. Comparative study of the histo‐physics of the aorta. Am. J. Physiol. 125: 1–14, 1939.
 175. Kramer, K., and U. C. Luft. Mobilization of red cells and oxygen from the spleen in severe hypoxia. Am. J. Physiol. 165: 215–228, 1951.
 176. Krogh, A. Regulation of the supply of blood to the right heart (with a description of a new circulation model). Skand. Arch. Physiol. 27: 227–248, 1912.
 177. Kügelgen, A. V. Über das Verhältnis von Ringmuskulatur und Innendruck in menschlichen grossen Venen. Z. Zellforsch. Mikroskop. Anat. 43: 168–183, 1955.
 178. Kuida, H. General relations of flow and pressure. Ann. NY Acad. Sci. 127: 364–372, 1965.
 179. Kumada, M., O. Okai, and A. Gunji. Mean circulatory pressure in carotid sinus reflex. Jap. J. Physiol. 21: 591–599, 1971.
 180. Landis, E. M. Capillary pressure and hyperemia in muscle and skin of the frog. Am. J. Physiol. 98: 704–716, 1931.
 181. Landis, E. M. Capillary pressure and capillary permeability. Physiol. Rev. 14: 404–481, 1934.
 182. Landis, E. M., and J. R. Pappenheimer. Exchange of substances through the capillary walls. In: Handbook of Physiology. Circulation, edited by W. F. Hamilton. Washington, DC: Am. Physiol. Soc., 1963, sect. 2, vol. II, chapt. 29, p. 961–1034.
 183. Learoyd, B. M., and M. G. Taylor. Alterations with age in the viscoelastic properties of human arterial walls. Circulation Res. 18: 287–292, 1965.
 184. Leonard, E., and S. J. Sarnoff. Effect of aramine‐induced smooth muscle contraction on length‐tension diagrams of venous strips. Circulation Res. 5: 169–174, 1957.
 185. Lesh, T. A., and C. F. Rothe. Sympathetic and hemodynamic effects on capacitance vessels in dog skeletal muscle. Am. J. Physiol. 217: 819–827, 1969.
 186. Levy, M. L., and L. Share. The influence of erythrocyte concentration upon the pressure‐flow relationships in the dog's hind limb. Circulation Res. 1: 247–255, 1953.
 187. Lipowsky, H. H., and B. W. Zweifach. Network analysis of microcirculation of cat mesentery. Microvascular Res. 7: 73–83, 1974.
 188. Longnecker, D., and F. L. Abel. Peripheral vascular response to stimulated haemorrhage shock during cardiopulmonary bypass in dogs. Circulation Res. 25: 107–117, 1969.
 189. Love, A. E. A Treatise on the Mathematical Theory of Elasticity. New York: Dover, 1944.
 190. Lundgren, O., J. Lundwall, and S. Mellander. Range of sympathetic discharge and reflex vascular adjustments in skeletal muscle during haemorrhagic hypotension. Acta Physiol. Scand. 62: 380–390, 1964.
 191. Lundvall, J. Tissue hyperosmolality as a mediator of vasodilatation and transcapillary fluid flux in exercising skeletal muscle. Acta Physiol. Scand. Suppl. 379: 1–142, 1972.
 192. Lundvall, J., S. Mellander, and H. Sparks. Myogenic response of resistance vessels and precapillary sphincters in skeletal muscle during exercise. Acta Physiol. Scand. 70: 257–268, 1967.
 193. Lundvall, J., S. Mellander, H. Westling, and T. White. Fluid transfer between blood and tissues during exercise. Acta Physiol. Scand. 85: 258–269, 1972.
 194. Mall, F. P. Die Blut und Lymphwege im Dünndarm des Hundes. Abhandl. Kgl. Sächs. Ges. Wiss. Math. Physik. K1. 1888, vol. 14. [Cited by Green et al. (122).]
 195. Mall, F. P. The architecture and blood vessels of the dog's spleen. Z. Morphol. Anthropol. 2: 1–42, 1900.
 196. Marty, A. T., and B. W. Zweifach. The splanchnic contribution to transcapillary refill after hemorrhagic shock. Ann. Surg. 174: 131–136, 1971.
 197. McDonald, D. A. Blood Flow in Arteries. London: Arnold, 1974.
 198. McDonald, D. A., and M. G. Taylor. The hydrodynamics of the arterial circulation. Progr. Biophys. Biophys. Chem. 9: 107–173, 1959.
 199. Mellander, S. Comparative studies on the adrenergic neural‐hormonal control of resistance and capacitance blood vessels in the cat. Acta. Physiol. Scand. 50: (Suppl. 176) 1–86, 1960.
 200. Mellander, S. Interaction of local and nervous factors in vascular control. Angiologia 8: 187–201, 1971.
 201. Mellander, S., and B. Johansson. Control of resistance, exchange and capacitance functions in the peripheral circulation. Pharmacol. Rev. 20: 117–196, 1968.
 202. Mellander, S., B. Johansson, S. Gray, O. Jonsson, J. Lundvall, and B. Ljung. The effects of hyperosmolality on intact and isolated vascular smooth muscle. Possible role in exercise hyperemia. Angiologica 4: 310–322, 1967.
 203. Mellander, S., and D. H. Lewis. Effect of hemorrhagic shock on the reactivity of resistance and capacitance vessels and on capillary filtration transfer in cat skeletal muscle. Circulation Res. 13: 105–118, 1963.
 204. Mellander, S., and B. Öberg. Transcapillary absorption and other vascular reactions in the human forearm during reduction of the circulating blood volume. Acta Physiol. Scand. 71: 37–46, 1967.
 205. Mellander, S., B. Öberg, and H. Odelram. Vascular adjustments to increased transmural pressure in cat and man with special reference to shifts in capillary fluid transfer. Acta Physiol. Scand. 61: 34–48, 1970.
 206. Merrill, E. W. Rheology of blood. Physiol. Rev. 49: 863–888, 1969.
 207. Milnor, W. R., D. H. Bergel, and J. D. Bargainer. Hydraulic power associated with pulmonary blood flow and its relation to heart rate. Circulation Res. 19: 467–480, 1966.
 208. Moens, A. I. Die Pulskurve. Leiden, 1878.
 209. Moreno, A. H., A. I. Katz, L. D. Gold, and R. V. Reddy. Mechanics of distension of dog veins and other very thin‐walled tubular structures. Circulation Res. 27: 1069–1079, 1970.
 210. Mountcastle, V. B. Medical Physiology. St. Louis: Mosby, 1974, vol. 2.
 211. Mozersky, D. J., D. S. Sumner, D. E. Hokanson, and D. E. Strandness. Transcutaneous measurement of the elastic properties of the human femoral artery. Circulation 46: 948–955, 1972.
 212. Nichol, J., F. Girling, W. Jerrard, E. B. Claxton, and A. C. Burton. Fundamental instability of the small blood vessels and critical closing pressures in vascular beds. Am. J. Physiol. 164: 330–344, 1951.
 213. Nichols, W. W., and D. A. McDonald. Wave velocity in the proximal aorta. Med. Biol. Eng. 10: 327–335, 1972.
 214. öberg, B. Effects of cardiovascular reflexes on net capillary transfer. Acta Physiol. Scand. 62: (Suppl. 229) 1–98, 1964.
 215. öberg, B. The relationship between active constriction and passive recoil of the veins at various distending pressures. Acta Physiol. Scand. 71: 233–247, 1967.
 216. öberg, B., R. Little, B. Rippe, and B. Folkow. The influence of rheological and collapse factors on pre‐ and postcapillary flow resistances in the skeletal muscle vascular bed of the cat. Acta Physiol. Scand. 95: 179–190, 1975.
 217. Oka, S., and T. Azuma. Physical theory of tension in thick‐walled blood vessels in equilibrium. Biorheology 7: 109–117, 1970.
 218. Olson, R. M., and D. K. Shelton, Jr. A nondestructive technique to measure wall displacement in the thoracic aorta. J. Appl. Physiol. 32: 147–151, 1972.
 219. O'Rourke, M. F. Pressure and flow waves in systemic arteries and the anatomical design of the arterial system. J. Appl. Physiol. 23: 139–149, 1967.
 220. O'Rourke, M. F. Steady and pulsatile energy losses in the systemic circulation under normal conditions and in simulated arterial disease. Cardiovascular Res. 1: 313–326, 1967.
 221. O'Rourke, M. F. Arterial haemodynamics in hypertension. Circulation Res. 26, 27: (Suppl. 2) 123–133, 1970.
 222. O'Rourke, M. F., and M. G. Taylor. Vascular impedance of the femoral bed. Circulation Res. 18: 126–139, 1966.
 223. O'Rourke, M. F., and M. G. Taylor. Input impedance of the systemic circulation. Circulation Res. 20: 365–380, 1967.
 224. Pace, J. B. Sympathetic control of pulmonary vascular impedance in anaesthetised dogs. Circulation Res. 24: 555–568, 1971.
 225. Pace, J. B., R. H. Cox, F. Alvarez‐Vara, and G. Karreman. Influence of sympathetic nerve stimulation on pulmonary hydraulic input power. Am. J. Physiol. 222: 196–201, 1972.
 226. Page, E. B., J. B. Hickam, H. O. Sieker, H. D. McIntosh, and W. W. Pryor. Reflex venomotor activity in normal persons and patients with postural hypotension. Circulation 11: 262–270, 1955.
 227. Pappenheimer, J. R., and A. Soto‐Rivera. Effective osmotic pressure of the plasma proteins and other quantities associated with the capillary circulation in the hindlimbs of cats and dogs. Am. J. Physiol. 152: 471–491, 1948.
 228. Patel, D. J., F. M. de Freitas, and D. L. Fry. Hydraulic input impedance to aorta and pulmonary artery in dogs. J. Appl. Physiol. 18: 134–140, 1963.
 229. Patel, D. J., F. M. de Freitas, J. C. Greenfield, Jr., and D. L. Fry. Relationship of radius to pressure along the aorta in living dogs. J. Appl. Physiol. 18: 1111–1117, 1963.
 230. Patel, D. J., and D. L. Fry. In situ pressure‐radius‐length measurements in ascending aorta of anesthetized dogs. J. Appl. Physiol. 19: 413–416, 1964.
 231. Patel, D. J., and D. L. Fry. The elastic symmetry of arterial segments in dogs. Circulation Res. 24: 1–8, 1969.
 232. Patel, D. J., J. S. Janicki, and T. E. Carew. Static anisotropic elastic properties of the aorta in living dogs. Circulation Res. 25: 765–779, 1969.
 233. Patel, D. J., D. P. Schilder, and A. J. Mallos. Mechanical properties and dimensions of the major pulmonary arteries. J. Appl. Physiol. 15: 92–96, 1960.
 234. Patel, D. J., and R. N. Vaishnav. The rheology of large blood vessels. In: Cardiovascular Fluid Dynamics, edited by D. H. Bergel. New York: Academic, 1972, vol II, p. 1–64.
 235. Peterson, L. H. Vessel wall stress‐strain relationship. In: Pulsatile Blood Flow, edited by E. O. Attinger. New York: McGraw‐Hill, 1964, p. 263–274.
 236. Peterson, L. H., R. E. Jensen, and J. Parnell. Mechanical properties of arteries in vivo. Circulation Res. 8: 622–639, 1960.
 237. Piene, H. The influence of pulmonary blood flow rate on vascular input impedance and hydraulic power in the sympathetically and noradrenaline stimulated cat lung. Acta. Physiol. Scand. 98: 44–53, 1976.
 238. Pieper, H. P., and L. T. Paul. Responses of aortic smooth muscle studied in intact dogs. Am. J. Physiol. 217: 154–160, 1969.
 239. Randall, J. E., and R. W. Stacy. Mechanical impedance of the dog's hind leg to pulsatile blood flow. Am. J. Physiol. 187: 94–98, 1956.
 240. Rees, P. M. Observations on the fine structure and distribution of presumptive baroreceptor nerves in the carotid sinus. J. Comp. Neurol. 131: 517–548, 1967.
 241. Rees, P. M. The distribution of biogenic amines in the carotid bifurcation region. J. Physiol. London 193: 245–253, 1967.
 242. Remington, J. W. Extensibility and hysteresis phenomena in smooth muscle tissues. In: Tissue Elasticity, edited by J. W. Remington. Washington, DC: Am. Physiol. Soc., 1957, p. 138–153.
 243. Remington, J. W. Propagation velocity of transient aortic pulses. Am. J. Physiol. 212: 612–618, 1967.
 244. Richardson, T. Q., J. O. Stallings, and A. C. Guyton. Pressure‐volume curves in live intact dogs. Am. J. Physiol. 201: 471–474, 1961.
 245. Roach, M. R., and A. C. Burton. The reason for the shape of the distensibility curves of arteries. Can. J. Biochem. Physiol. 35: 681–690, 1957.
 246. Ross, J. Jr., C. J. Frahm, and E. Braunwald. Influence of carotid baroreceptors and vasoactive drugs on systemic vascular and venous distensibility. Circulation Res. 9: 75–82, 1961.
 247. Rothe, C. F., and J. A. Drees. Vascular capacitance and fluid shifts during prolonged haemorrhagic hypotension. Circulation Res. 38: 347–356, 1976.
 248. Rowell, L. B. Human cardiovascular adjustments to exercise and thermal stress. Physiol. Rev. 54: 75–159, 1974.
 249. Rowell, L. B. The splanchnic circulation. In: Physiology and Biophysics, edited by T. C. Ruch and H. D. Patton. Philadelphia: Saunders, 1974, vol. II, p. 229.
 250. Roy, C. S. The elastic properties of the arterial wall. J. Physiol. London 3: 125–162, 1880.
 251. Roy, C. S. The physiology and pathology of the spleen. J. Physiol. London 3: 203–228, 1881.
 252. Ruch, T. C., and H. D. Patton. Physiology and Biophysics. Philadelphia: Saunders, 1974, vol. II.
 253. Rushmer, R. F. Cardiovascular Dynamics. Philadelphia: Saunders, 1976.
 254. Rushmer, R. F., and O. A. Smith, Jr. Cardiac control. Physiol. Rev. 39: 41–68, 1959.
 255. Sagawa, K. Analysis of ventricular pumping capacity as a function of input and output pressure loads. In: Physical Basis of Circulatory Transport: Regulation and Exchange, edited by E. B. Reeve and A. C. Guyton. Philadelphia: Saunders, 1968, p. 141–149.
 256. Sagawa, K., M. Kumada, and L. P. Schramm. Nervous Control of the circulation. In: Cardiovascular Physiology, edited by A. C. Guyton and C. E. Jones. London: Butterworths, 1974, vol. 1, p. 197–232. (Intern. Rev. Physiol. Ser.)
 257. Saltin, B., and J. Stenberg. Circulatory response to prolonged severe exercise. J. Appl. Physiol. 19: 833–838, 1964.
 258. Sarnoff, S. J., J. H. Mitchell, J. P. Gilmore, and J. P. Remensnyder. Homeometric autoregulation in the heart. Circulation Res. 8: 1077–1091, 1960.
 259. Schiff, M. Über die Function der Milz. Lecons sur la physiologie de la digestion tII, XXXV leçon, 416–452, 1867. [Cited by Grayson and Mendel (116), p. 147.]
 260. Schmidt‐Schönbein, H. Microbiology of erythrocytes, blood viscosity and the distribution of blood flow in the microcirculation. In: Cardiovascular Physiology II, edited by A. C. Guyton and A. W. Cowley. Baltimore: Univ. Park, 1976, vol. 9, p. 1–62. (Intern. Rev. Physiol. Ser.)
 261. Schretzenmayr, A. Die Motorik des intaken Venesystems. II. Nachweis und Bedeutung der Hohlvenenmotorik. Arch. Expt. Pathol. Pharmak. 180: 295–311, 1936.
 262. Schwinghamer, J. M., G. J. Grega, and F. J. Haddy. Skin and muscle circulatory responses during prolonged hypovolemia. Am. J. Physiol. 219: 318–326, 1970.
 263. Shadle, O. W., M. Zukof, and J. Diana. Translocation of blood from the isolated dog's hind limb during levarterenol infusion and sciatic nerve stimulation. Circulation Res. 6: 326–333, 1958.
 264. Shapiro, H. M., D. D. Stromberg, D. R. Lee, and C. A. Wiederhielm. Dynamic pressures in the pial arterial microcirculation. Am. J. Physiol. 221: 279–283, 1971.
 265. Shepherd, J. T. Physiology of the Circulation in Human Limbs in Health and Disease. Philadelphia: Saunders, 1963.
 266. Shepherd, J. T. Role of the veins in the circulation. Circulation 33: 484–491, 1966.
 267. Shoukas, A. A., and K. Sagawa. Total systemic vascular compliance measured as incremental volume‐pressure ratio. Circulation Res. 28: 277–289, 1971.
 268. Shoukas, A. A., and K. Sagawa. Control of total systemic vascular capacity by the carotid sinus baroreceptor reflex. Circulation Res. 33: 22–33, 1973.
 269. Smaje, L., B. W. Zweifach, and M. Intaglietta. Micropressures and capillary filtration coefficients in single vessels of the cremaster muscle of the rat. Microvasc. Res. 2: 96–110, 1970.
 270. Somlyo, A. P., and A. V. Somlyo. Vascular smooth muscle. I. Normal structure pathology, biochemistry and biophysics. Pharmacol. Rev. 20: 197–272, 1968.
 271. Sonnenblick, E. H., and S. E. Downing. Afterload as a primary determinant of ventricular performance. Am. J. Physiol. 204: 604–610, 1963.
 272. Sparks, H. V., Jr., and D. F. Bohr. Effect of stretch on passive tension and contractility of isolated vascular smooth muscles. Am. J. Physiol. 202: 835–840, 1962.
 273. Speden, R. N. The effect of initial strip length on the nor‐adrenaline‐induced isometric contraction of arterial strips. J. Physiol. London 154: 15–25, 1960.
 274. Speden, R. N. The maintenance of arterial constriction at different transmural pressures. J. Physiol. London 229: 361–381, 1973.
 275. Speden, R. N. Muscle load and constriction of the rabbit ear artery. J. Physiol. London 248: 531–553, 1975.
 276. Speden, R. N., and D. J. Freckelton. Constriction of arteries at high transmural pressures. Circulation Res. 26, 27: (Suppl. 2) 99–112, 1970.
 277. Starling, E. H. On the absorption of fluids from the connective tissue spaces. J. Physiol. London 19: 312–326, 1896.
 278. Strey, W., W. Schwartzkopff, W. Wurm, and H. Freishius. Bestimmung der Weitbarkeit des System‐, des Intraund Extrathorakalkreislaufes beim Menchen nach kontrolliertem Blutverlust. Verh. Dtsch. Ges. Kreislaufforsch. 39: 248–252, 1973. [Cited by Gauer and Henry (99).]
 279. Stukeley, W. On the Spleen, its Description and History, With Their Remedy. London, 1723.
 280. Tafür, E., and W. G. Guntheroth. Simultaneous pressure, flow and diameter of the vena cava with fright and exercise. Circulation Res. 19: 42–50, 1966.
 281. Taylor, M. G. An experimental determination of the propagation of fluid oscillations in a tube with a viscoelastic wall; together with an analysis of the characteristics required in an electrical analog. Phys. Med. Biol. 4: 63–82, 1959.
 282. Taylor, M. G. Wave travel in arteries and the design of the cardiovascular system. In: Pulsatile Blood Flow, edited by E. O. Attinger. New York: McGraw‐Hill, 1964, p. 343–372.
 283. Taylor, M. G. Wave travel in a non‐uniform transmission line, in relation to pulses in arteries. Phys. Med. Biol. 10: 539–50, 1965.
 284. Taylor, M. G. The input impedance of an assembly of randomly branching elastic tubes. Biophys. J. 6: 29–51, 1966.
 285. Taylor, M. G. Use of random excitation and spectral analysis in the study of frequency‐dependent parameters of the cardiovascular system. Circulation Res. 18: 585–595, 1966.
 286. Thoenen, H., A. Hürlimann, and W. Haefely. The effect of postganglionic stimulation on the isolated, perfused spleen of the cat. Helv. Physiol. Pharmacol. Acta 21: 17–26, 1963.
 287. Thron, H. L., and K. D. Scheppokat. Tunusänderungen peripherer kapazitiver Gefässe. Verh. Dtsch. Ges. Kreislaufforsch. 24: 333–338, 1958.
 288. Tickner, E. G., and A. H. Sacks. Theoretical and experimental study of the elastic behavior of the human brachial and other human and canine arteries. Vidya Report 162, California, Itek Corp.
 289. Timoshenko, S. P., and J. N. Goodier. Theory of Elasticity. Tokyo: McGraw‐Hill, Kogakusha, 1970.
 290. Ungewiss, U. Kreislaufuntersungen bei essentieller Hypertension unter besonderer Beruchsichtigung des Niederdrucksystems. Inaugural dissertation, Berlin, 1969. [Cited by Gauer and Henry (99).]
 291. Van Citters, R. L. Occlusion of lumina in small arterioles during vasoconstriction. Circulation Res. 18: 199–204, 1966.
 292. Van Citters, R. L., B. M. Wagner, and R. F. Rushmer. Architecture of small arteries during vasoconstriction. Circulation Res. 10: 668–675, 1962.
 293. Vanhoutte, P. M., and J. T. Shepherd. Effect of temperature on reactivity of isolated cutaneous veins of the dog. Am. J. Physiol. 218: 187–190, 1970.
 294. Wagner, R. Nachrichtembl. Gestame Wiss (Göttingen) no. 8, 89–96, 1849. [Cited by Davies and Witherington (72), p. 380.]
 295. Wallentin, I. Studies on intestinal circulation. Acta Physiol. Scand. Suppl. 279: 1–38, 1966.
 296. Watson, W. E. Action of aminophiline on venous distensibility. Clin. Sci. 22: 22–65, 1962.
 297. Webb‐Pebloe, M. M., and J. T. Shepherd. Response of dog's cutaneous veins to local and central temperature changes. Circulation Res. 23: 693–699, 1968.
 298. Webb‐Pebloe, M. M., and J. T. Shepherd. Responses of the superficial limbs vein of the dog to changes in temperature. Circulation Res. 22: 737–746, 1968.
 299. Wetterer, E., and T. Kenner. Grundlagen der Dynamik des Arterienpulses. Berlin: Springer, 1968.
 300. Whittaker, S. R. F., and F. R. Winton. The apparent viscosity of blood flowing in the isolated hind limb of the dog and its variation with corpuscular concentration. J. Physiol. London 78: 339–369, 1933.
 301. Wiedeman, M. P. Dimensions of blood vessels from distributing artery to collecting vein. Circulation Res. 12: 375–378, 1963.
 302. Wiederhielm, C. A. Distensibility characteristics of small blood vessels. Federation Proc. 24: 1075–1084, 1965.
 303. Wiederhielm, C. A., J. W. Woodbury, S. Kirk, and R. F. Rushmer. Pulsatile pressures in the microcirculation of frog's mesentery. Am. J. Physiol. 207: 173–176, 1964.
 304. Wolinsky, H., and S. Glagov. A lamellar unit of aortic medial structure and function in mammals. Circulation Res. 20: 99–111, 1967.
 305. Womersley, J. R. Oscillatory flow in arteries: the constrained elastic tube as a model of arterial flow and pulse transmission. Phys. Med. Biol. 2: 178–187, 1957.
 306. Wood, J. E., and J. W. Eckstein. A tandem forearm plethysmograph for study of acute responses of the peripheral veins of man: the effect of environmental and local temperature change, and the effect of environmental and local temperature change, and the effect of pooling blood in the extremities. J. Clin. Invest. 37: 41–50, 1958.

Contact Editor

Submit a note to the editor about this article by filling in the form below.

* Required Field

Article Title: Circulatory Correlates: Vascular Impedance, Resistance, and Capacity
 

How to Cite

Barry S. Gow. Circulatory Correlates: Vascular Impedance, Resistance, and Capacity. Compr Physiol 2011, Supplement 7: Handbook of Physiology, The Cardiovascular System, Vascular Smooth Muscle: 353-408. First published in print 1980. doi: 10.1002/cphy.cp020214