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Effect of Local Metabolic Factors on Vascular Smooth Muscle

Harvey V. Sparks

10.1002/cphy.cp020217

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 Oxygen
1.1 Effect
1.2 Mechanisms of Action
1.3 Situations in Which O2 Tension in Vessel Wall May Influence Vascular Tone
2 Potassium Ion
2.1 Effect
2.2 Mechanisms of Action
2.3 Situations in Which Vessel Wall [K+] May Influence Vascular Tone
3 Osmolarity
3.1 Effect
3.2 Mechanisms of Action
3.3 Situations in Which Changes in Tissue Vessel Wall Osmolarity May Influence Vascular Tone
Figure 1. Figure 1.

Change in canine vascular resistance (forelimb, kidney, and heart) and ventricular contractile force as a function of low arterial blood Po2. Arterial blood is passed through an isolated, ventilated lung. Graded changes in Po2 accomplished by altering gas mixture used to ventilate lung.

From Daugherty et al. 52
Figure 2. Figure 2.

Changes in perivascular Po2 caused by superfusing a hamster cheek pouch preparation with low (Po2 = 11 mmHg), intermediate (Po2 = 47 mmHg), and high (Po2 = 84 mmHg) Po2 solution. Hatched bars indicate changes observed when solution was changed from low to intermediate Po2; open bars indicate effect of changing from low to high Po2. Values are shown as means ± SE. Numbers in the bars are number of experiments performed. Asterisks indicate a significant difference was detected with Student's t test at 5% level of confidence.

From Duling 60, by permission of the American Heart Association, Inc
Figure 3. Figure 3.

Relation of Po2 to contractile tension developed by rabbit aortic strip in response to 3 μg/l epinephrine (Epi). Specific oxygen tensions are indicated by numbers on Po2 tracing.

From Detar and Bohr 56
Figure 4. Figure 4.

A: relation of critical solution Po2 to square of one‐half rabbit aortic strip thickness, a2. Each point represents one experiment. Least‐squares regression line is shown. B: relation of critical solution Po2 (P8c) to a′2. The a′ is a measure of strip thickness that takes into account width of strips. This offers another dimension for diffusion of O2. See Ref. 231 for further explanation. Each point represents one experiment. Equation for least‐squares regression line and the correlation coefficient are given. These plots suggest that diffusion distance, a, is the primary variable influencing critical Po2 and that for a sufficiently thin strip the critical Po2 would be close to that of mitochondria. The point X is from Fay (76.

From Pittman and Duling 231
Figure 5. Figure 5.

Effect of graded reductions in bath Po2 and increases in bath [CN−] on oxygen consumption (2) and tension developments in rabbit aortic strips. A: active tension caused by norepinephrine. B: active tension caused by K+. Maximum oxygen uptake and tension development were not different for K+ and norepinephrine. Note that norepinephrine‐induced tension is much more sensitive to reductions in bath Po2 than is K+‐induced tension. Cyanide has less effect on tension for a given o2 than does Po2 when the agonist is norepinephrine. These results suggest that a factor other than oxidative phosphorylation is involved in response of rabbit aorta to lowered bath Po2, especially when tension is produced by norepinephrine.

From Coburn 46
Figure 6. Figure 6.

Isolated pulmonary arterial and aortic strips were incubated in a muscle bath at Po2 20 mmHg for 4 h. Epinephrine was then added to bath (vertical arrow). When bath Po2 was lowered to near zero, pulmonary strip contracted and aorta relaxed. Raising bath Po2 caused pulmonary strip to relax and aortic strip to contract.

From Detar and Gellai 58
Figure 7. Figure 7.

Skeletal muscle blood flow (MF) and venous Po2 when dogs were breathing 1 atm room air (control) compared with dogs breathing 100% oxygen under 2 atm pressure. Note that MF curve remains within control area. The venous Po2 curve, however, is well above, and is no longer similar in shape to its room‐air control, suggesting that in this case autoregulation of flow is not dependent on oxygen tension. ΔP is local perfusion pressure minus venous pressure.

From Bond et al. 27
Figure 8. Figure 8.

Autoregulatory response of skeletal muscle flow to reduction in perfusion pressure. A: under normal conditions. B: during mild hypoxia. Note smaller change in flow for a given decrease in pressure during mild hypoxia. This suggests that resistance vessels are sensitive to lowered tissue perfusion if tissue Po2 is sufficiently low. PA, iliac artery pressure; PV, iliac vein pressure; A‐V/ΔO2, arteriovenous oxygen difference; FA, iliac artery flow; o2,muscle oxygen uptake; Pvo2, iliac vein oxygen tension; Kf,capillary filtration coefficient.

From Granger et al. 101, by permission of the American Heart Association, Inc
Figure 9. Figure 9.

Relation between oxygen consumption and blood flow, □; venous Po2, ○; and venous hemoglobin saturation, Δ, of denervated canine skeletal muscle. Various O2 consumptions produced by twitch rates ranging from 0.25 to 8/s.

From Sparks 264
Figure 10. Figure 10.

Average time course of changes in coronary sinus O2 content and coronary vascular resistance. A: after a step increase in heart rate. B: after a step decrease in heart rate. To compare time courses of these two variables, it is necessary to take into account the delay and dispersion between capillary changes in O2 content and the venous measurement site. This was done by convoluting the changes in vascular resistance with dye curve estimates of venous transit, so that both coronary sinus O2 content and vascular resistance are subjected to the same delay and dispersion. When this is done, changes in coronary sinus O2 precede changes in coronary vascular resistance. Because flow was held constant, changes in oxygen consumption preceded changes in vascular resistance. *, Convolution integral has been applied to these data.

From Belloni and Sparks 12
Figure 11. Figure 11.

Model used to calculate arteriolar wall Po2 based on values for O2 flux across vascular wall, Jo2; permeability‐surface area product for O2 for the vessel wall, PS; Po2 within the vessel, Po2N and Po2 in tissue surrounding the arteriole, . Given flow through the vessel, F, and O2 content of blood, [O2]N‐1, the delivery of O2 into an arteriolar segment can be calculated. The exit of O2 from a segment is the sum of the flow removal, F[O2]N, and the flux across the wall, Jo2. Wall Po2 for any segment can be calculated from the resting Po2 gradient across the wall, Δ, and the ratio of the flux in a given condition, , to the resting O2 flux, . Values for most parameters and variables were taken from or derived from data supplied by Duling 66. Changes in flow and tissue Po2 were estimated from changes in flow and venous Po2 associated with exercise of canine skeletal muscles (see Fig. 9).
Figure 12. Figure 12.

Results of simulated graded exercise using model in Figure 11. Flow and venous Po2 values were used as inputs. Average wall Po2, obtained by averaging the wall Po2's of each segment, decreases with small increases in oxygen consumption because the fall in tissue Po2, reflected by venous Po2, has more influence on wall Po2 than the increased flow delivery of O2. But once oxygen consumption is above ∼5 ml/min · 100 g the increased flow delivery of O2 dominates and arteriolar wall Po2 increases. The qualitative point is that arteriolar wall Po2 does not necessarily decrease during exercise because it is maintained by increased flow delivery of O2.
Figure 13. Figure 13.

Effects of 40 μmol isosmotic KCl injected into the circumflex coronary artery. A: effect on aortic blood pressure, heart rate, and mean circumflex blood flow. B: effect on aortic blood pressure and pulsatile circumflex blood flow. Increase in end‐diastolic flow (B) indicates that the increased flow is not the result of decreased ventricular force of contractions.

From Murray and Sparks 217, by permission of the American Heart Association, Inc
Figure 14. Figure 14.

Comparison of effects of KCl on response of rabbit aorta and mesoappendix ‘arteriole’ to epinephrine. Increase in bath [K+] from 4.7 mM to 10 mM caused contraction of aorta and relaxation of the smaller vessel.

From Bohr and Goulet 24
Figure 15. Figure 15.

Simultaneous records of contraction and 3H efflux during exposure to K+‐free physiologic saline solution (time enclosed by arrows). The 3H efflux was shown to represent efflux of [3H]norepinephrine. When K+ is replaced, relaxation precedes reduction in efflux of 3H. The washout delay of the system is shown by open circles, indicating that slower decrease in 3H efflux is not an artifact of washout. Because relaxation occurs faster than decrease in 3H release, it appears that relaxation is not the result of reduced norepinephrine release.

From Bonaccorsi et al. 25
Figure 16. Figure 16.

Actions of K+ concentration and Ba2+ on resting membrane potential (Em) and input resistance (rin). A: resting Em did not reach slope of 60 mV/decade in solutions with normal Cl− and without Ba2+ (circles, solid line); slope was decreased by Ba2+ both in normal Cl− (triangles, solid line) and in low Cl− (squares, broken line) solutions. All lines extrapolate to a zero‐potential intercept of 160 mM. Standard errors for potential measurements were less than 2 mV and thus are not shown. B: rin decreased with higher [K+]o in all solutions. At lower [K+]o, Ba2+ increased rin in both normal and low [Cl−]o solutions. Symbols reflect same solutions described in A. All curves are drawn by approximation. Standard errors are shown for normal solutions and solutions with Ba2+ and normal Cl−, but not in solutions with low Cl− to avoid confusion (n = 26–43 for each point). All measurements were made 2–10 min after a [K+]o change.

From Hermsmeyer 133
Figure 17. Figure 17.

Effect of increasing [K]o from 3.18 mM to 7.18 mM during agonist‐induced contractile response. A: coronary strips stimulated with acetylcholine. B: deep femoral arterial strips stimulated with norepinephrine. In both strips, potassium‐induced relaxation was followed by recovery of tension back to the prerelaxation level within 5 min. Tension reached a new steady‐state level above control in each strip.

From Gellai and Detar 92, by permission of the American Heart Association, Inc
Figure 18. Figure 18.

Average effects of prolonged heavy exercise of dog gracilis muscle on resistance (RDG), flow (FDG), Po2, pH, Pco2, [K+], and osmolality (Osm) of venous blood. Note that although flow remains elevated (dots above error bars indicate statistical significance when compared to control) and resistance remains decreased during the entire 1‐h stimulation period, venous [K+] and osmolarlity return to near starting values.

From Stowe et al. 269
Figure 19. Figure 19.

Time course of interstitial [K+], calculated from data in Reference 213, compared to time course of vascular conductance of skeletal muscle following a 1‐s period of tetanus at zero time. Change in interstitial [K+] precedes change in vascular conductance. This suggests that elevated [K+] is a cause of vasodilation that follows brief periods of tetanus.
Figure 20. Figure 20.

Tension and perfusion pressure (at constant flow) of isolated skeletal muscle preparations from a control dog and a dog depleted of K+ by dietary restriction. Note that muscle of K+‐depleted dog developed less tension and exhibited less vasodilation with elimination of second phase of initial vasodilator response. Circled numbers indicate phases of vasodilator response.

From Hazeyama and Sparks 122
Figure 21. Figure 21.

Left coronary artery blood flow of a dog was reduced in steps as indicated by number at top of figure. Change in coronary vascular resistance reaches a minimum value at 22 min, but K+ release began to dramatically increase only after that. This result suggests that K+ release does not play a role in autoregulation of coronary blood flow. Lactate refers to arterial and venous blood concentration of lactate. S‐T refers to changes in S‐T segment of electrocardiogram from isoelectric value.

From Case et al. 41
Figure 22. Figure 22.

Changes in arterial pressure (AP) and femoral flow (Q) of dog in response to intra‐arterial infusions of hypertonic sucrose, glucose, or urea. Note peak transit response which then returns toward control levels. Flow remains elevated in response to sucrose and glucose, but not to urea. Infusion began at ↑ and stopped at ↓.

From Stainsby and Barclay 265, by permission of the American Heart Association, Inc
Figure 23. Figure 23.

Effects of hyperosmotic solutions on spontaneous mechanical activity of rat portal vein. Period in hyperosmotic solution indicated by bar. Note that reduced frequency of contraction as well as reduced tension development are transient and in the case of urea, both variables return to base‐line values.

From Johansson and Jonsson 151
Figure 24. Figure 24.

Effect of hyperosmolarity on spontaneous contractions of rat portal vein. Period in hyperosmolar medium is indicated by bar. A: addition of 40 mmol NaCl/l medium. B: addition of 80 mmol sucrose/l medium. C: addition of 80 mmol urea/l medium. Note that initial reduction in rate and amplitude of contractions is soon replaced by elevated contractile force.

From McKinley et al. 201
Figure 25. Figure 25.

Diagram showing blood flow in cat skeletal muscle (ml/min‐100 g at perfusion pressure of 100 mmHg) during exercise and during intra‐arterial infusion of hypertonic solutions plotted against corresponding increases in venous osmolality. Note that for a given increase in venous osmolality the increase in steady‐state vascular conductance during infusion of hyperosmotic solutions is less than 50% of the increase in conductance observed during exercise.

From Lundvall 191
Figure 26. Figure 26.

Vascular resistance of dog skeletal muscle plotted as a function of venous osmolarity during exercise and infusion of hypertonic solutions. At both 1 and 5 min after initiation of exercise (indicated by 1 and 5), there is a relatively large decrease in resistance and little increase in venous osmolarity.

From Scott et al. 250


Figure 1.

Change in canine vascular resistance (forelimb, kidney, and heart) and ventricular contractile force as a function of low arterial blood Po2. Arterial blood is passed through an isolated, ventilated lung. Graded changes in Po2 accomplished by altering gas mixture used to ventilate lung.

From Daugherty et al. 52


Figure 2.

Changes in perivascular Po2 caused by superfusing a hamster cheek pouch preparation with low (Po2 = 11 mmHg), intermediate (Po2 = 47 mmHg), and high (Po2 = 84 mmHg) Po2 solution. Hatched bars indicate changes observed when solution was changed from low to intermediate Po2; open bars indicate effect of changing from low to high Po2. Values are shown as means ± SE. Numbers in the bars are number of experiments performed. Asterisks indicate a significant difference was detected with Student's t test at 5% level of confidence.

From Duling 60, by permission of the American Heart Association, Inc


Figure 3.

Relation of Po2 to contractile tension developed by rabbit aortic strip in response to 3 μg/l epinephrine (Epi). Specific oxygen tensions are indicated by numbers on Po2 tracing.

From Detar and Bohr 56


Figure 4.

A: relation of critical solution Po2 to square of one‐half rabbit aortic strip thickness, a2. Each point represents one experiment. Least‐squares regression line is shown. B: relation of critical solution Po2 (P8c) to a′2. The a′ is a measure of strip thickness that takes into account width of strips. This offers another dimension for diffusion of O2. See Ref. 231 for further explanation. Each point represents one experiment. Equation for least‐squares regression line and the correlation coefficient are given. These plots suggest that diffusion distance, a, is the primary variable influencing critical Po2 and that for a sufficiently thin strip the critical Po2 would be close to that of mitochondria. The point X is from Fay (76.

From Pittman and Duling 231


Figure 5.

Effect of graded reductions in bath Po2 and increases in bath [CN−] on oxygen consumption (2) and tension developments in rabbit aortic strips. A: active tension caused by norepinephrine. B: active tension caused by K+. Maximum oxygen uptake and tension development were not different for K+ and norepinephrine. Note that norepinephrine‐induced tension is much more sensitive to reductions in bath Po2 than is K+‐induced tension. Cyanide has less effect on tension for a given o2 than does Po2 when the agonist is norepinephrine. These results suggest that a factor other than oxidative phosphorylation is involved in response of rabbit aorta to lowered bath Po2, especially when tension is produced by norepinephrine.

From Coburn 46


Figure 6.

Isolated pulmonary arterial and aortic strips were incubated in a muscle bath at Po2 20 mmHg for 4 h. Epinephrine was then added to bath (vertical arrow). When bath Po2 was lowered to near zero, pulmonary strip contracted and aorta relaxed. Raising bath Po2 caused pulmonary strip to relax and aortic strip to contract.

From Detar and Gellai 58


Figure 7.

Skeletal muscle blood flow (MF) and venous Po2 when dogs were breathing 1 atm room air (control) compared with dogs breathing 100% oxygen under 2 atm pressure. Note that MF curve remains within control area. The venous Po2 curve, however, is well above, and is no longer similar in shape to its room‐air control, suggesting that in this case autoregulation of flow is not dependent on oxygen tension. ΔP is local perfusion pressure minus venous pressure.

From Bond et al. 27


Figure 8.

Autoregulatory response of skeletal muscle flow to reduction in perfusion pressure. A: under normal conditions. B: during mild hypoxia. Note smaller change in flow for a given decrease in pressure during mild hypoxia. This suggests that resistance vessels are sensitive to lowered tissue perfusion if tissue Po2 is sufficiently low. PA, iliac artery pressure; PV, iliac vein pressure; A‐V/ΔO2, arteriovenous oxygen difference; FA, iliac artery flow; o2,muscle oxygen uptake; Pvo2, iliac vein oxygen tension; Kf,capillary filtration coefficient.

From Granger et al. 101, by permission of the American Heart Association, Inc


Figure 9.

Relation between oxygen consumption and blood flow, □; venous Po2, ○; and venous hemoglobin saturation, Δ, of denervated canine skeletal muscle. Various O2 consumptions produced by twitch rates ranging from 0.25 to 8/s.

From Sparks 264


Figure 10.

Average time course of changes in coronary sinus O2 content and coronary vascular resistance. A: after a step increase in heart rate. B: after a step decrease in heart rate. To compare time courses of these two variables, it is necessary to take into account the delay and dispersion between capillary changes in O2 content and the venous measurement site. This was done by convoluting the changes in vascular resistance with dye curve estimates of venous transit, so that both coronary sinus O2 content and vascular resistance are subjected to the same delay and dispersion. When this is done, changes in coronary sinus O2 precede changes in coronary vascular resistance. Because flow was held constant, changes in oxygen consumption preceded changes in vascular resistance. *, Convolution integral has been applied to these data.

From Belloni and Sparks 12


Figure 11.

Model used to calculate arteriolar wall Po2 based on values for O2 flux across vascular wall, Jo2; permeability‐surface area product for O2 for the vessel wall, PS; Po2 within the vessel, Po2N and Po2 in tissue surrounding the arteriole, . Given flow through the vessel, F, and O2 content of blood, [O2]N‐1, the delivery of O2 into an arteriolar segment can be calculated. The exit of O2 from a segment is the sum of the flow removal, F[O2]N, and the flux across the wall, Jo2. Wall Po2 for any segment can be calculated from the resting Po2 gradient across the wall, Δ, and the ratio of the flux in a given condition, , to the resting O2 flux, . Values for most parameters and variables were taken from or derived from data supplied by Duling 66. Changes in flow and tissue Po2 were estimated from changes in flow and venous Po2 associated with exercise of canine skeletal muscles (see Fig. 9).



Figure 12.

Results of simulated graded exercise using model in Figure 11. Flow and venous Po2 values were used as inputs. Average wall Po2, obtained by averaging the wall Po2's of each segment, decreases with small increases in oxygen consumption because the fall in tissue Po2, reflected by venous Po2, has more influence on wall Po2 than the increased flow delivery of O2. But once oxygen consumption is above ∼5 ml/min · 100 g the increased flow delivery of O2 dominates and arteriolar wall Po2 increases. The qualitative point is that arteriolar wall Po2 does not necessarily decrease during exercise because it is maintained by increased flow delivery of O2.



Figure 13.

Effects of 40 μmol isosmotic KCl injected into the circumflex coronary artery. A: effect on aortic blood pressure, heart rate, and mean circumflex blood flow. B: effect on aortic blood pressure and pulsatile circumflex blood flow. Increase in end‐diastolic flow (B) indicates that the increased flow is not the result of decreased ventricular force of contractions.

From Murray and Sparks 217, by permission of the American Heart Association, Inc


Figure 14.

Comparison of effects of KCl on response of rabbit aorta and mesoappendix ‘arteriole’ to epinephrine. Increase in bath [K+] from 4.7 mM to 10 mM caused contraction of aorta and relaxation of the smaller vessel.

From Bohr and Goulet 24


Figure 15.

Simultaneous records of contraction and 3H efflux during exposure to K+‐free physiologic saline solution (time enclosed by arrows). The 3H efflux was shown to represent efflux of [3H]norepinephrine. When K+ is replaced, relaxation precedes reduction in efflux of 3H. The washout delay of the system is shown by open circles, indicating that slower decrease in 3H efflux is not an artifact of washout. Because relaxation occurs faster than decrease in 3H release, it appears that relaxation is not the result of reduced norepinephrine release.

From Bonaccorsi et al. 25


Figure 16.

Actions of K+ concentration and Ba2+ on resting membrane potential (Em) and input resistance (rin). A: resting Em did not reach slope of 60 mV/decade in solutions with normal Cl− and without Ba2+ (circles, solid line); slope was decreased by Ba2+ both in normal Cl− (triangles, solid line) and in low Cl− (squares, broken line) solutions. All lines extrapolate to a zero‐potential intercept of 160 mM. Standard errors for potential measurements were less than 2 mV and thus are not shown. B: rin decreased with higher [K+]o in all solutions. At lower [K+]o, Ba2+ increased rin in both normal and low [Cl−]o solutions. Symbols reflect same solutions described in A. All curves are drawn by approximation. Standard errors are shown for normal solutions and solutions with Ba2+ and normal Cl−, but not in solutions with low Cl− to avoid confusion (n = 26–43 for each point). All measurements were made 2–10 min after a [K+]o change.

From Hermsmeyer 133


Figure 17.

Effect of increasing [K]o from 3.18 mM to 7.18 mM during agonist‐induced contractile response. A: coronary strips stimulated with acetylcholine. B: deep femoral arterial strips stimulated with norepinephrine. In both strips, potassium‐induced relaxation was followed by recovery of tension back to the prerelaxation level within 5 min. Tension reached a new steady‐state level above control in each strip.

From Gellai and Detar 92, by permission of the American Heart Association, Inc


Figure 18.

Average effects of prolonged heavy exercise of dog gracilis muscle on resistance (RDG), flow (FDG), Po2, pH, Pco2, [K+], and osmolality (Osm) of venous blood. Note that although flow remains elevated (dots above error bars indicate statistical significance when compared to control) and resistance remains decreased during the entire 1‐h stimulation period, venous [K+] and osmolarlity return to near starting values.

From Stowe et al. 269


Figure 19.

Time course of interstitial [K+], calculated from data in Reference 213, compared to time course of vascular conductance of skeletal muscle following a 1‐s period of tetanus at zero time. Change in interstitial [K+] precedes change in vascular conductance. This suggests that elevated [K+] is a cause of vasodilation that follows brief periods of tetanus.



Figure 20.

Tension and perfusion pressure (at constant flow) of isolated skeletal muscle preparations from a control dog and a dog depleted of K+ by dietary restriction. Note that muscle of K+‐depleted dog developed less tension and exhibited less vasodilation with elimination of second phase of initial vasodilator response. Circled numbers indicate phases of vasodilator response.

From Hazeyama and Sparks 122


Figure 21.

Left coronary artery blood flow of a dog was reduced in steps as indicated by number at top of figure. Change in coronary vascular resistance reaches a minimum value at 22 min, but K+ release began to dramatically increase only after that. This result suggests that K+ release does not play a role in autoregulation of coronary blood flow. Lactate refers to arterial and venous blood concentration of lactate. S‐T refers to changes in S‐T segment of electrocardiogram from isoelectric value.

From Case et al. 41


Figure 22.

Changes in arterial pressure (AP) and femoral flow (Q) of dog in response to intra‐arterial infusions of hypertonic sucrose, glucose, or urea. Note peak transit response which then returns toward control levels. Flow remains elevated in response to sucrose and glucose, but not to urea. Infusion began at ↑ and stopped at ↓.

From Stainsby and Barclay 265, by permission of the American Heart Association, Inc


Figure 23.

Effects of hyperosmotic solutions on spontaneous mechanical activity of rat portal vein. Period in hyperosmotic solution indicated by bar. Note that reduced frequency of contraction as well as reduced tension development are transient and in the case of urea, both variables return to base‐line values.

From Johansson and Jonsson 151


Figure 24.

Effect of hyperosmolarity on spontaneous contractions of rat portal vein. Period in hyperosmolar medium is indicated by bar. A: addition of 40 mmol NaCl/l medium. B: addition of 80 mmol sucrose/l medium. C: addition of 80 mmol urea/l medium. Note that initial reduction in rate and amplitude of contractions is soon replaced by elevated contractile force.

From McKinley et al. 201


Figure 25.

Diagram showing blood flow in cat skeletal muscle (ml/min‐100 g at perfusion pressure of 100 mmHg) during exercise and during intra‐arterial infusion of hypertonic solutions plotted against corresponding increases in venous osmolality. Note that for a given increase in venous osmolality the increase in steady‐state vascular conductance during infusion of hyperosmotic solutions is less than 50% of the increase in conductance observed during exercise.

From Lundvall 191


Figure 26.

Vascular resistance of dog skeletal muscle plotted as a function of venous osmolarity during exercise and infusion of hypertonic solutions. At both 1 and 5 min after initiation of exercise (indicated by 1 and 5), there is a relatively large decrease in resistance and little increase in venous osmolarity.

From Scott et al. 250
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Article Title: Effect of Local Metabolic Factors on Vascular Smooth Muscle
 

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Harvey V. Sparks. Effect of Local Metabolic Factors on Vascular Smooth Muscle. Compr Physiol 2011, Supplement 7: Handbook of Physiology, The Cardiovascular System, Vascular Smooth Muscle: 475-513. First published in print 1980. doi: 10.1002/cphy.cp020217