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Arterial Baroreflexes in Humans

Giuseppe Mancia, Allyn L. Mark

10.1002/cphy.cp020320

Source: Supplement 8: Handbook of Physiology, The Cardiovascular System, Peripheral Circulation and Organ Blood Flow

Originally published: 1983

Published online: January 2011

Full Article on Wiley Online Library



Abstract

The sections in this article are:

1 Techniques
1.1 Carotid Sinus Massage
1.2 Electrical Stimulation of Carotid Sinus Nerves
1.3 Section or Anesthesia of Carotid Sinus Nerves and Vagi
1.4 Occlusion of Common Carotid Arteries
1.5 Neck Chamber
1.6 Vasoactive Drugs
1.7 Nonselective Techniques
2 Arterial Baroreceptor Control of Heart Rate
2.1 Autonomic Mediation
2.2 Other Properties
2.3 Relationship to Base‐Line R‐R Interval
2.4 Relationship to Respiratory Cycle
3 Arterial Baroreceptor Control of Atrioventricular Conduction and Ventricles
4 Carotid Baroreceptor Control of Blood Pressure
5 Carotid Baroreceptor Influence on Cardiac Output and Total Peripheral Resistance
6 Arterial Baroreceptor Control of Regional Circulations
7 Arterial Baroreceptor Control of Veins
8 Set Point of Carotid Baroreflex
9 Aortic Baroreflexes
10 Factors That Modify Arterial Baroreceptor Control of Circulation
10.1 Age
10.2 Exercise
10.3 Mental Stress
10.4 Sleep
10.5 Anesthesia
10.6 Central Blood Volume and Posture
11 Pathological States
11.1 Hypertension
11.2 Heart Disease
11.3 Carotid Sinus Syndrome
11.4 Other Pathological Conditions
12 Modification of Arterial Baroreflexes by Drugs
12.1 β‐Adrenergic Antagonists
12.2 Cardiac Glycosides
12.3 Antihypertensive Drugs
Figure 1. Figure 1.

Simultaneous record of pressure changes in 1 subject in neck chamber, in tissue adjacent to carotid sinus, in internal jugular vein at level of carotid sinus, and in cervical esophagus. Time trace, 5‐s and 1‐s intervals. Measurements in internal jugular vein were made to validate tissue‐pressure measurements.

From Ludbrook et al. 204
Figure 2. Figure 2.

Effects of carotid baroreceptor stimuli applied at different times before appearance of P wave on heart (P‐P) interval. •, Response to each stimulus; ○, averages obtained at 0.2‐s intervals. Baroreceptor stimuli induced by neck suction of 60 mmHg for 0.58‐s duration. Data from 1 subject.

From Eckberg 94
Figure 3. Figure 3.

Effects of carotid baroreceptor stimuli for 5 s on P‐P interval. •, Responses to single stimuli; ▴, averages obtained at 0.5‐s intervals. Baroreceptor stimuli induced by neck suctions of 50 mmHg. Data from 1 subject.

From Eckberg 96
Figure 4. Figure 4.

Prolongation of P‐P interval evoked by electrical stimulation of carotid sinus nerves for 300 ms. •, Values during or after stimulation; ○, control values in absence of stimulation. Stimulation time indicated by vertical lines immediately below ordinate. Means ± SE from several observations.

From Borst and Karemaker 44
Figure 5. Figure 5.

Effects on P‐P interval of carotid baroreceptor stimuli applied at 6 different times during respiratory cycle. Baroreceptor stimuli induced by neck suction of 30 mmHg for 0.6 s. Heart interval responses calculated by subtracting maximal effects during stimulation from base‐line values in absence of stimulation. Data are means ± SE for 6 subjects.

From Eckberg et al. 103
Figure 6. Figure 6.

A: marked depression of increase in heart (R‐R) interval induced by carotid baroreceptor stimulation during hypocapnic hyperventilation. B: lesser depression induced by hyperventilation during isocapnia. From top: tidal volume (v); heart period (H.P.); endtidal O2; endtidal PCO2 (CO2); pressure within neck chamber (mmHg). Neck suction stimuli 1 and 4 applied before and after hyperventilation during resting breathing. Stimuli 2 and 3 applied during hypocapnic hyperventilation, stimulus 5 during isocapnic hyperventilation with increased tidal volume, and stimulus 6 during isocapnic hyperventilation with even more increased tidal volume.

From Trzebski et al. 323
Figure 7. Figure 7.

Effects of phenylephrine‐induced increases in mean arterial pressure on R‐R, A‐H, and H‐V intervals. Means ± SE from 11 subjects studied for sinus rhythm and during atrial pacing. C, control values; PHE, values during plateau increase in mean arterial pressure induced by phenylephrine.

From Mancia et al. 207, by permission of the American Heart Association, Inc
Figure 8. Figure 8.

Effects of trinitroglycerin‐induced reductions in mean arterial pressure on R‐R, A‐H, and H‐V intervals. Means ± SE from 9 subjects studied for sinus rhythm (top) and during atrial pacing (bottom). C, control values; TNG, values during plateau decrease in mean arterial pressure induced by trinitroglycerin.

From Mancia et al. 207, by permission of the American Heart Association, Inc
Figure 9. Figure 9.

Effect of bilateral compression of common carotid artery. Data from 1 subject.

From Roddie and Shepherd 273
Figure 10. Figure 10.

Unloading of both cardiopulmonary and arterial baroreceptors [lower‐body negative pressure (LBNP) at −40 mmHg] increased both forearm and splanchnic vascular resistances. Simultaneous application of neck suction (NS), performed to minimize decrease in carotid transmural pressure and thus the contribution of carotid baroreflex during LBNP, prevented most splanchnic vasoconstriction but did not significantly attenuate forearm vasoconstriction during LBNP. Results indicate that cardiopulmonary receptors have major influence on forearm vessels, whereas carotid baroreceptors have major influence on splanchnic vessels in humans.

Adapted from Abboud et al. 2
Figure 11. Figure 11.

Bursts of muscle sympathetic efferent traffic (upper trace) during oscillations in arterial blood pressure (lower trace). More bursts occurred during decreasing than during increasing blood pressure values when latency for reflex sympathetic modulation (1.3 s) was taken into account.

From Sundlöf and Wallin 310
Figure 12. Figure 12.

Increase in pressure induced by phenylephrine (upper traces) and reduction in pressure induced by bradykinin (lower traces) accompanied by bradycardia and tachycardia, respectively, but by no change in tone of cutaneous veins. Right panel shows reactivity of veins by constriction after deep inspiration. Each line, 1 normal subject.

From Epstein et al. 108, by copyright permission of The American Society for Clinical Investigation
Figure 13. Figure 13.

Changes in mean arterial pressure (MAP) induced by changes in neck tissue pressure (NTP) outside carotid sinuses. Data are means ± SE of individual regression coefficients in 11 normal subjects for sustained responses to steady neck chamber pressure or suction applications.

From Mancia et al. 214, by permission of the American Heart Association, Inc
Figure 14. Figure 14.

Changes in heart interval (R‐R interval) with drug‐induced alterations in mean arterial pressure (MAP) and with neck chamber‐induced alterations in carotid transmural pressure (CTP). Means (solid lines) ± SE (dashed lines) of individual regression coefficients taken from 8 normal subjects in whom both techniques were used. Maximal heart interval responses were considered for neck chamber, with changes in CTP calculated by subtracting changes in MAP from changes in tissue pressure outside carotid sinuses. Method described by Korner et al. 184 was used for drug technique. Control MAP and heart interval were 101 ± 5 mmHg and 864 ± 61 ms, respectively, for drug studies and 105 ± 5 mmHg and 791 ± 59 ms for neck chamber studies.

From Mancia et al. 214, by permission of the American Heart Association, Inc
Figure 15. Figure 15.

Effect of age on baroreflex sensitivity in normotensive and hypertensive subjects. Baroreflex sensitivity expressed (vertical line) as logarithm of slope relating increase in R‐R interval and rise in systolic blood pressure induced by phenylephrine.

From Gribbin et al. 138, by permission of the American Heart Association, Inc
Figure 16. Figure 16.

Relationship between mean arterial pressure and heart period (R‐R interval) in a group of younger (top) and older (bottom) subjects. Each group includes normotensive, moderately hypertensive, and severely hypertensive subjects. Stimulus‐response curves constructed by increasing (phenylephrine injection) or decreasing (trinitroglycerin injection) mean arterial pressure from base‐line value (large black circle) and by calculating heart interval during steady‐state phase of response. Data are means ± SE for several subjects

From Korner et al. 184
Figure 17. Figure 17.

Effects of carotid baroreceptor stimulation by neck suction on hemodynamic variables at different levels of dynamic leg exercise in supine position. Data are means for 6 normal subjects. Note well‐preserved blood pressure reductions during baroreceptor stimulation. Heart rate reductions also evident but with some attenuation at greatest exercise level.

From Bevegård and Shepherd 32, by copyright permission of The American Society for Clinical Investigation
Figure 18. Figure 18.

Slope of linear regression (lines) between increases in systolic blood pressure induced by phenylephrine and resulting lengthening in pulse interval (R‐R) interval. Data from several subjects studied at rest and at progressively increasing work loads (dynamic exercise). Slopes of baroreflex control of heart interval progressively diminish and flatten at greatest exercise levels.

From Bristow et al. 53, by permission of the American Heart Association, Inc
Figure 19. Figure 19.

Changes in sensitivity of baroreceptor‐heart rate reflex during wakefulness‐sleep cycle in 1 subject. Sensitivity calculated from slope of increase in R‐R interval in response to systolic pressure rise induced by angiotensin injections. Arrows, times of injection; •, slopes. Diagram shows systolic, diastolic, and sometimes mean blood pressure (○) values. Bottom, electroencephalogram (EEG) patterns: greatest level, wakefulness (W); lowest level, rapid‐eye‐movement (REM) sleep; and intermediate levels, slow‐sleep stages (I, II, III, IV).

From Smyth et al. 307, by permission of the American Heart Association, Inc
Figure 20. Figure 20.

A: prolongation of pulse interval caused by neck suction in 8 supine subjects before (•) and after (▴) propranolol. B: responses of 5 standing subjects before (•) and after (▴) propranolol.

From Eckberg, Abboud, and Mark 99
Figure 21. Figure 21.

Slope of linear regression (lines) between increases in systolic pressure (mmHg) induced by angiotensin and resulting lengthening of R‐R interval. Data from normal subject (A) and hypertensive subject (B).

From Bristow et al. 55, by permission of the American Heart Association, Inc
Figure 22. Figure 22.

Carotid baroreceptor influence on blood pressure in 11 normotensive (○), 18 moderately hypertensive (•), 17 severely hypertensive (X) subjects ± SE for mean arterial pressure during control period in each group, respectively. Solid line represents mean of individual regression coefficients relating mean arterial pressure to increased and decreased carotid transmural pressure with respect to control values; dashed lines indicate standard errors of regressions. Data are shown for steady‐state effects of neck chamber, with carotid transmural pressure calculated as difference between mean arterial pressure and tissue pressure outside carotid sinuses. Latter was calculated from variation in value of neck chamber pressure after application of correction factors for loss of pressure transmission through neck tissues.

From Mancia et al. 218, by permission of the American Heart Association, Inc
Figure 23. Figure 23.

Sensitivity of baroreceptor‐heart rate reflex during arterial baroreceptor stimulation by phenylephrine and arterial baroreceptor deactivation by trinitroglycerin before and after intravenous administration of 0.8 mg lanatoside C. Sensitivity expressed by regression coefficient of relationship between changes in R‐R interval (ms) and changes in systolic arterial pressure. Data are means ± SE.

From Ferrari et al. 115, by permission of the American Heart Association, Inc
Figure 24. Figure 24.

Changes in mean arterial pressure (MAP) and R‐R interval (HI) induced by carotid baroreceptor stimulation (neck suction, top) and carotid baroreceptor inhibition (neck pressure application, bottom). C, control values; E, early response to variations in neck pressure; SS, steady‐state response to neck chamber variations. Mean values ± SE from 7 subjects, P values refer to differences in response before and after 0.8 mg lanatoside C.

From Ferrari et al. 115, by permission of the American Heart Association, Inc


Figure 1.

Simultaneous record of pressure changes in 1 subject in neck chamber, in tissue adjacent to carotid sinus, in internal jugular vein at level of carotid sinus, and in cervical esophagus. Time trace, 5‐s and 1‐s intervals. Measurements in internal jugular vein were made to validate tissue‐pressure measurements.

From Ludbrook et al. 204


Figure 2.

Effects of carotid baroreceptor stimuli applied at different times before appearance of P wave on heart (P‐P) interval. •, Response to each stimulus; ○, averages obtained at 0.2‐s intervals. Baroreceptor stimuli induced by neck suction of 60 mmHg for 0.58‐s duration. Data from 1 subject.

From Eckberg 94


Figure 3.

Effects of carotid baroreceptor stimuli for 5 s on P‐P interval. •, Responses to single stimuli; ▴, averages obtained at 0.5‐s intervals. Baroreceptor stimuli induced by neck suctions of 50 mmHg. Data from 1 subject.

From Eckberg 96


Figure 4.

Prolongation of P‐P interval evoked by electrical stimulation of carotid sinus nerves for 300 ms. •, Values during or after stimulation; ○, control values in absence of stimulation. Stimulation time indicated by vertical lines immediately below ordinate. Means ± SE from several observations.

From Borst and Karemaker 44


Figure 5.

Effects on P‐P interval of carotid baroreceptor stimuli applied at 6 different times during respiratory cycle. Baroreceptor stimuli induced by neck suction of 30 mmHg for 0.6 s. Heart interval responses calculated by subtracting maximal effects during stimulation from base‐line values in absence of stimulation. Data are means ± SE for 6 subjects.

From Eckberg et al. 103


Figure 6.

A: marked depression of increase in heart (R‐R) interval induced by carotid baroreceptor stimulation during hypocapnic hyperventilation. B: lesser depression induced by hyperventilation during isocapnia. From top: tidal volume (v); heart period (H.P.); endtidal O2; endtidal PCO2 (CO2); pressure within neck chamber (mmHg). Neck suction stimuli 1 and 4 applied before and after hyperventilation during resting breathing. Stimuli 2 and 3 applied during hypocapnic hyperventilation, stimulus 5 during isocapnic hyperventilation with increased tidal volume, and stimulus 6 during isocapnic hyperventilation with even more increased tidal volume.

From Trzebski et al. 323


Figure 7.

Effects of phenylephrine‐induced increases in mean arterial pressure on R‐R, A‐H, and H‐V intervals. Means ± SE from 11 subjects studied for sinus rhythm and during atrial pacing. C, control values; PHE, values during plateau increase in mean arterial pressure induced by phenylephrine.

From Mancia et al. 207, by permission of the American Heart Association, Inc


Figure 8.

Effects of trinitroglycerin‐induced reductions in mean arterial pressure on R‐R, A‐H, and H‐V intervals. Means ± SE from 9 subjects studied for sinus rhythm (top) and during atrial pacing (bottom). C, control values; TNG, values during plateau decrease in mean arterial pressure induced by trinitroglycerin.

From Mancia et al. 207, by permission of the American Heart Association, Inc


Figure 9.

Effect of bilateral compression of common carotid artery. Data from 1 subject.

From Roddie and Shepherd 273


Figure 10.

Unloading of both cardiopulmonary and arterial baroreceptors [lower‐body negative pressure (LBNP) at −40 mmHg] increased both forearm and splanchnic vascular resistances. Simultaneous application of neck suction (NS), performed to minimize decrease in carotid transmural pressure and thus the contribution of carotid baroreflex during LBNP, prevented most splanchnic vasoconstriction but did not significantly attenuate forearm vasoconstriction during LBNP. Results indicate that cardiopulmonary receptors have major influence on forearm vessels, whereas carotid baroreceptors have major influence on splanchnic vessels in humans.

Adapted from Abboud et al. 2


Figure 11.

Bursts of muscle sympathetic efferent traffic (upper trace) during oscillations in arterial blood pressure (lower trace). More bursts occurred during decreasing than during increasing blood pressure values when latency for reflex sympathetic modulation (1.3 s) was taken into account.

From Sundlöf and Wallin 310


Figure 12.

Increase in pressure induced by phenylephrine (upper traces) and reduction in pressure induced by bradykinin (lower traces) accompanied by bradycardia and tachycardia, respectively, but by no change in tone of cutaneous veins. Right panel shows reactivity of veins by constriction after deep inspiration. Each line, 1 normal subject.

From Epstein et al. 108, by copyright permission of The American Society for Clinical Investigation


Figure 13.

Changes in mean arterial pressure (MAP) induced by changes in neck tissue pressure (NTP) outside carotid sinuses. Data are means ± SE of individual regression coefficients in 11 normal subjects for sustained responses to steady neck chamber pressure or suction applications.

From Mancia et al. 214, by permission of the American Heart Association, Inc


Figure 14.

Changes in heart interval (R‐R interval) with drug‐induced alterations in mean arterial pressure (MAP) and with neck chamber‐induced alterations in carotid transmural pressure (CTP). Means (solid lines) ± SE (dashed lines) of individual regression coefficients taken from 8 normal subjects in whom both techniques were used. Maximal heart interval responses were considered for neck chamber, with changes in CTP calculated by subtracting changes in MAP from changes in tissue pressure outside carotid sinuses. Method described by Korner et al. 184 was used for drug technique. Control MAP and heart interval were 101 ± 5 mmHg and 864 ± 61 ms, respectively, for drug studies and 105 ± 5 mmHg and 791 ± 59 ms for neck chamber studies.

From Mancia et al. 214, by permission of the American Heart Association, Inc


Figure 15.

Effect of age on baroreflex sensitivity in normotensive and hypertensive subjects. Baroreflex sensitivity expressed (vertical line) as logarithm of slope relating increase in R‐R interval and rise in systolic blood pressure induced by phenylephrine.

From Gribbin et al. 138, by permission of the American Heart Association, Inc


Figure 16.

Relationship between mean arterial pressure and heart period (R‐R interval) in a group of younger (top) and older (bottom) subjects. Each group includes normotensive, moderately hypertensive, and severely hypertensive subjects. Stimulus‐response curves constructed by increasing (phenylephrine injection) or decreasing (trinitroglycerin injection) mean arterial pressure from base‐line value (large black circle) and by calculating heart interval during steady‐state phase of response. Data are means ± SE for several subjects

From Korner et al. 184


Figure 17.

Effects of carotid baroreceptor stimulation by neck suction on hemodynamic variables at different levels of dynamic leg exercise in supine position. Data are means for 6 normal subjects. Note well‐preserved blood pressure reductions during baroreceptor stimulation. Heart rate reductions also evident but with some attenuation at greatest exercise level.

From Bevegård and Shepherd 32, by copyright permission of The American Society for Clinical Investigation


Figure 18.

Slope of linear regression (lines) between increases in systolic blood pressure induced by phenylephrine and resulting lengthening in pulse interval (R‐R) interval. Data from several subjects studied at rest and at progressively increasing work loads (dynamic exercise). Slopes of baroreflex control of heart interval progressively diminish and flatten at greatest exercise levels.

From Bristow et al. 53, by permission of the American Heart Association, Inc


Figure 19.

Changes in sensitivity of baroreceptor‐heart rate reflex during wakefulness‐sleep cycle in 1 subject. Sensitivity calculated from slope of increase in R‐R interval in response to systolic pressure rise induced by angiotensin injections. Arrows, times of injection; •, slopes. Diagram shows systolic, diastolic, and sometimes mean blood pressure (○) values. Bottom, electroencephalogram (EEG) patterns: greatest level, wakefulness (W); lowest level, rapid‐eye‐movement (REM) sleep; and intermediate levels, slow‐sleep stages (I, II, III, IV).

From Smyth et al. 307, by permission of the American Heart Association, Inc


Figure 20.

A: prolongation of pulse interval caused by neck suction in 8 supine subjects before (•) and after (▴) propranolol. B: responses of 5 standing subjects before (•) and after (▴) propranolol.

From Eckberg, Abboud, and Mark 99


Figure 21.

Slope of linear regression (lines) between increases in systolic pressure (mmHg) induced by angiotensin and resulting lengthening of R‐R interval. Data from normal subject (A) and hypertensive subject (B).

From Bristow et al. 55, by permission of the American Heart Association, Inc


Figure 22.

Carotid baroreceptor influence on blood pressure in 11 normotensive (○), 18 moderately hypertensive (•), 17 severely hypertensive (X) subjects ± SE for mean arterial pressure during control period in each group, respectively. Solid line represents mean of individual regression coefficients relating mean arterial pressure to increased and decreased carotid transmural pressure with respect to control values; dashed lines indicate standard errors of regressions. Data are shown for steady‐state effects of neck chamber, with carotid transmural pressure calculated as difference between mean arterial pressure and tissue pressure outside carotid sinuses. Latter was calculated from variation in value of neck chamber pressure after application of correction factors for loss of pressure transmission through neck tissues.

From Mancia et al. 218, by permission of the American Heart Association, Inc


Figure 23.

Sensitivity of baroreceptor‐heart rate reflex during arterial baroreceptor stimulation by phenylephrine and arterial baroreceptor deactivation by trinitroglycerin before and after intravenous administration of 0.8 mg lanatoside C. Sensitivity expressed by regression coefficient of relationship between changes in R‐R interval (ms) and changes in systolic arterial pressure. Data are means ± SE.

From Ferrari et al. 115, by permission of the American Heart Association, Inc


Figure 24.

Changes in mean arterial pressure (MAP) and R‐R interval (HI) induced by carotid baroreceptor stimulation (neck suction, top) and carotid baroreceptor inhibition (neck pressure application, bottom). C, control values; E, early response to variations in neck pressure; SS, steady‐state response to neck chamber variations. Mean values ± SE from 7 subjects, P values refer to differences in response before and after 0.8 mg lanatoside C.

From Ferrari et al. 115, by permission of the American Heart Association, Inc
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Article Title: Arterial Baroreflexes in Humans
 

How to Cite

Giuseppe Mancia, Allyn L. Mark. Arterial Baroreflexes in Humans. Compr Physiol 2011, Supplement 8: Handbook of Physiology, The Cardiovascular System, Peripheral Circulation and Organ Blood Flow: 755-793. First published in print 1983. doi: 10.1002/cphy.cp020320