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Cardiopulmonary Baroreflexes in Humans

Allyn L. Mark, Giuseppe Mancia

10.1002/cphy.cp020321

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 Lower‐Body Negative Pressure
1.2 Congesting Cuffs and Hemorrhage
1.3 Elevation of Legs and Lower‐Body Positive Pressure
1.4 Head‐Out Water Immersion
1.5 Upright Tilting and Respiratory Maneuvers
2 Cardiopulmonary Baroreceptor Control of Forearm Vascular Resistance and Sympathetic Nerve Activity
3 Cardiopulmonary Baroreceptor Control of Splanchnic Circulation
4 Cardiopulmonary Baroreceptor Control of Venous Tone
5 Cardiopulmonary Baroreceptor Control of Heart Rate
6 Cardiopulmonary Baroreceptor Control of Renin and Vasopressin
6.1 Renin Release
6.2 Vasopressin Secretion
7 Interaction of Cardiopulmonary, Carotid, and Somatic Reflexes
8 Myocardial Ischemia and Infarction
8.1 Mechanisms of Bradycardia and Hypotension With Inferoposterior Infarction
8.2 Mechanisms of Tachycardia and Hypertension With Anterior Myocardial Infarction
9 Pathological States
9.1 Bradycardia and Hypotension During Coronary Arteriography
9.2 Chronic Heart Failure
9.3 Hypertension
9.4 Syncope
Figure 1. Figure 1.

Responses to lower‐body negative pressure (LBNP) at 10 and 40 mmHg. At 10 mmHg, LBNP decreases central venous pressure without decreasing arterial pulse pressure or mean pressure, thus inhibiting cardiopulmonary but not arterial baroreceptors. This is accompanied by reflex forearm vasoconstriction without reflex tachycardia. At 40 mmHg, LBNP decreases both central venous pressure and arterial pulse pressure, thus inhibiting both cardiopulmonary and arterial baroreceptors, which produces slight further forearm vasoconstriction and increases heart rate.

From Abboud and Mark 2
Figure 2. Figure 2.

Average values for responses to ramp lower‐body negative pressure (LBNP) in 9 subjects. MP, mean pressure; PP, pulse pressure; RAP, right atrial pressure; HR, heart rate; SBF, splanchnic blood flow; and FBF, forearm blood flow. Ramp LBNP applied at −1 mmHg/min. Bars with entries for SBF indicate SE; values for SE for other variables were too small to be shown. Asterisks denote first 3 significant decrements in SBF below control. At 0‐20 mmHg, LBNP decreased RAP without decreasing aortic MP or PP and without increasing HR. This mild LBNP produced substantial decreases in FBF and slight decreases in SBF. At 20‐50 mmHg, LBNP decreased aortic PP and RAP and produced increases in HR, further decreases in SBF and FBF.

From Johnson et al. 70, by permission of the American Heart Association, Inc
Figure 3. Figure 3.

Changes in number and amplitude of bursts of sympathetic nerve activity in muscle branches of median nerve in humans during graded lower‐body negative pressure (LBNP). Mild LBNP, which inhibits cardiopulmonary but not arterial baroreceptors, increased number and amplitude of sympathetic bursts. Increase in sympathetic activity in muscles was not related to changes in arterial pressure.

Adapted from Sundlöf and Wallin 106
Figure 4. Figure 4.

Effect of water immersion to neck on plasma renin activity (PRA) in subjects in balance on a 10‐meq sodium diet. Immersion resulted in progressive decrement in PRA beginning as early as 30 min. Cessation of immersion was associated with prompt return of PRA to prestudy values. Serial measurements obtained in control state without immersion did not reveal decrease in PRA.

From Epstein et al. 41
Figure 5. Figure 5.

Plasma renin and hemodynamic responses to inflation and deflation of congesting thigh cuffs. PRA, plasma renin activity; BP, intra‐arterial blood pressure; RAP, right atrial pressure; and HR, heart rate. Inflation of thigh‐congesting cuffs decreased RAP and increased PRA and HR without measured decreases in BP.

Adapted from Kiowski and Julius 73
Figure 6. Figure 6.

Effects of head‐up tilting (dashed lines) and application of positive pressure in neck chamber (continuous lines) in 5 patients. PRA, plasma renin activity; v — a, venous‐arterial difference. Results shown as mean values ± SE in control state (C) and during 5th min of tilting or positive neck pressure (S). Unloading of cardiopulmonary and arterial baroreceptors with tilting increased v — a of PRA. In contrast, selective unloading of carotid baroreceptors with neck pressure increased mean arterial pressure but did not significantly increase v — a of PRA.

From Mancia et al. 80
Figure 7. Figure 7.

Plasma levels of arginine vasopressin (AVP) during control study and during 4 h of water immersion. Values are mean ± SE. During control study, mean plasma AVP was unchanged throughout 6 h of observation. In contrast, immersion caused prompt suppression of AVP, which was sustained throughout the 4‐h period of immersion.

From Epstein et al. 42
Figure 8. Figure 8.

Interaction of cardiopulmonary and somatic reflexes in humans. Figure shows increases in forearm vascular resistance in mmHg · ml−1 · min−1 · 100 ml−1 forearm volume during lower‐body negative pressure (LBNP) at −5 mmHg, during sustained handgrip at 10% and 20% maximum voluntary contraction, and during combined handgrip and LBNP. Values in parentheses indicate corresponding changes in mean arterial pressure. Handgrip and LBNP each produced modest increases in forearm vascular resistance. A threefold potentiation of forearm vasoconstrictor response to sustained handgrip was produced by LBNP. This increase in resistance was significantly greater than sum of increase in resistance resulting from separate LBNP or handgrip.

Adapted from Walker et al. 115
Figure 9. Figure 9.

Changes in heart rate during anterior wall and inferior wall ischemia in patients with coronary spasm and Prinzmetal's angina. Heart rate increased during anterior wall ischemia and decreased during inferior wall ischemia.

Adapted from Perez‐Gomez et al. 92
Figure 10. Figure 10.

Changes in forearm blood flow (A) and forearm vascular resistance (B) produced by injection of 8 ml of Hypaque‐M 75% into left coronary artery. Arrows indicate injections. Coronary injection of contrast medium caused prompt increases in forearm blood flow and decreases in forearm vascular resistance.

From Zelis et al. 122, by permission of the American Heart Association, Inc
Figure 11. Figure 11.

Comparison of decreases in sinus heart rate during right coronary artery (RCA) versus left coronary artery (LCA) injections of contrast medium in patients with obviously dominant RCA circulation, so that RCA injections supplied the inferoposterior wall and LCA injections supplied the anterolateral wall. Magnitude of sinus slowing was greater with RCA injections supplying the inferoposterior wall of left ventricle.

From Perez‐Gomez et al. 91
Figure 12. Figure 12.

Forearm vascular responses to lower‐body negative pressure (LBNP) and neck pressure in borderline hypertensive (BHT) and normotensive (NT) subjects. Forearm vasoconstrictor responses to LBNP were augmented, whereas forearm vasoconstrictor responses to neck pressure were impaired in BHT subjects. Thus there is support for augmentation of cardiopulmonary baroreflexes and impairment in carotid baroreflexes in young BHT men.

From Mark and Kerber 84, by permission of the American Heart Association, Inc
Figure 13. Figure 13.

Pathophysiological consequences of proposed abnormalities in arterial and cardiopulmonary baroreflex control in borderline hypertensive subjects. Impairment in arterial baroreflex inhibition of vasomotor centers would be expected to increase sympathetic activity and renin, but in supine position, augmentation of cardiopulmonary baroreflex inhibition of vasomotor center modulates expected increases in sympathetic activity and renin. With standing, however, decreases in cardiac filling pressure remove augmented cardiopulmonary baroreflex inhibition and permit impairment in arterial baroreceptor inhibition of vasomotor center to be expressed as augmented postural increases in sympathetic activity and renin.
Figure 14. Figure 14.

Hypothesized role of stimulation of left ventricular baroreceptors during exercise in patients with severe aortic stenosis. Top: afferent impulses originating in exercising leg muscles normally produce reflex vasoconstriction in nonexercising forearm. In patients with severe aortic stenosis, increases in left ventricular pressure activate left ventricular baroreceptors, which inhibit and reverse forearm vasoconstriction and may promote exertional syncope.

From Mark et al. 85, by copyright permission of The American Society for Clinical Investigation
Figure 15. Figure 15.

Forearm vascular responses to supine leg exercise in patient with severe calcific aortic stenosis before and after aortic valve replacement. Before operation (solid lines and dots) patient displayed abnormal forearm vasodilator response in leg exercise. After operation (dashed lines and circles) patient displayed normal forearm vasoconstrictor response to leg exercise.

From Mark et al. 85, by copyright permission of The American Society for Clinical Investigation


Figure 1.

Responses to lower‐body negative pressure (LBNP) at 10 and 40 mmHg. At 10 mmHg, LBNP decreases central venous pressure without decreasing arterial pulse pressure or mean pressure, thus inhibiting cardiopulmonary but not arterial baroreceptors. This is accompanied by reflex forearm vasoconstriction without reflex tachycardia. At 40 mmHg, LBNP decreases both central venous pressure and arterial pulse pressure, thus inhibiting both cardiopulmonary and arterial baroreceptors, which produces slight further forearm vasoconstriction and increases heart rate.

From Abboud and Mark 2


Figure 2.

Average values for responses to ramp lower‐body negative pressure (LBNP) in 9 subjects. MP, mean pressure; PP, pulse pressure; RAP, right atrial pressure; HR, heart rate; SBF, splanchnic blood flow; and FBF, forearm blood flow. Ramp LBNP applied at −1 mmHg/min. Bars with entries for SBF indicate SE; values for SE for other variables were too small to be shown. Asterisks denote first 3 significant decrements in SBF below control. At 0‐20 mmHg, LBNP decreased RAP without decreasing aortic MP or PP and without increasing HR. This mild LBNP produced substantial decreases in FBF and slight decreases in SBF. At 20‐50 mmHg, LBNP decreased aortic PP and RAP and produced increases in HR, further decreases in SBF and FBF.

From Johnson et al. 70, by permission of the American Heart Association, Inc


Figure 3.

Changes in number and amplitude of bursts of sympathetic nerve activity in muscle branches of median nerve in humans during graded lower‐body negative pressure (LBNP). Mild LBNP, which inhibits cardiopulmonary but not arterial baroreceptors, increased number and amplitude of sympathetic bursts. Increase in sympathetic activity in muscles was not related to changes in arterial pressure.

Adapted from Sundlöf and Wallin 106


Figure 4.

Effect of water immersion to neck on plasma renin activity (PRA) in subjects in balance on a 10‐meq sodium diet. Immersion resulted in progressive decrement in PRA beginning as early as 30 min. Cessation of immersion was associated with prompt return of PRA to prestudy values. Serial measurements obtained in control state without immersion did not reveal decrease in PRA.

From Epstein et al. 41


Figure 5.

Plasma renin and hemodynamic responses to inflation and deflation of congesting thigh cuffs. PRA, plasma renin activity; BP, intra‐arterial blood pressure; RAP, right atrial pressure; and HR, heart rate. Inflation of thigh‐congesting cuffs decreased RAP and increased PRA and HR without measured decreases in BP.

Adapted from Kiowski and Julius 73


Figure 6.

Effects of head‐up tilting (dashed lines) and application of positive pressure in neck chamber (continuous lines) in 5 patients. PRA, plasma renin activity; v — a, venous‐arterial difference. Results shown as mean values ± SE in control state (C) and during 5th min of tilting or positive neck pressure (S). Unloading of cardiopulmonary and arterial baroreceptors with tilting increased v — a of PRA. In contrast, selective unloading of carotid baroreceptors with neck pressure increased mean arterial pressure but did not significantly increase v — a of PRA.

From Mancia et al. 80


Figure 7.

Plasma levels of arginine vasopressin (AVP) during control study and during 4 h of water immersion. Values are mean ± SE. During control study, mean plasma AVP was unchanged throughout 6 h of observation. In contrast, immersion caused prompt suppression of AVP, which was sustained throughout the 4‐h period of immersion.

From Epstein et al. 42


Figure 8.

Interaction of cardiopulmonary and somatic reflexes in humans. Figure shows increases in forearm vascular resistance in mmHg · ml−1 · min−1 · 100 ml−1 forearm volume during lower‐body negative pressure (LBNP) at −5 mmHg, during sustained handgrip at 10% and 20% maximum voluntary contraction, and during combined handgrip and LBNP. Values in parentheses indicate corresponding changes in mean arterial pressure. Handgrip and LBNP each produced modest increases in forearm vascular resistance. A threefold potentiation of forearm vasoconstrictor response to sustained handgrip was produced by LBNP. This increase in resistance was significantly greater than sum of increase in resistance resulting from separate LBNP or handgrip.

Adapted from Walker et al. 115


Figure 9.

Changes in heart rate during anterior wall and inferior wall ischemia in patients with coronary spasm and Prinzmetal's angina. Heart rate increased during anterior wall ischemia and decreased during inferior wall ischemia.

Adapted from Perez‐Gomez et al. 92


Figure 10.

Changes in forearm blood flow (A) and forearm vascular resistance (B) produced by injection of 8 ml of Hypaque‐M 75% into left coronary artery. Arrows indicate injections. Coronary injection of contrast medium caused prompt increases in forearm blood flow and decreases in forearm vascular resistance.

From Zelis et al. 122, by permission of the American Heart Association, Inc


Figure 11.

Comparison of decreases in sinus heart rate during right coronary artery (RCA) versus left coronary artery (LCA) injections of contrast medium in patients with obviously dominant RCA circulation, so that RCA injections supplied the inferoposterior wall and LCA injections supplied the anterolateral wall. Magnitude of sinus slowing was greater with RCA injections supplying the inferoposterior wall of left ventricle.

From Perez‐Gomez et al. 91


Figure 12.

Forearm vascular responses to lower‐body negative pressure (LBNP) and neck pressure in borderline hypertensive (BHT) and normotensive (NT) subjects. Forearm vasoconstrictor responses to LBNP were augmented, whereas forearm vasoconstrictor responses to neck pressure were impaired in BHT subjects. Thus there is support for augmentation of cardiopulmonary baroreflexes and impairment in carotid baroreflexes in young BHT men.

From Mark and Kerber 84, by permission of the American Heart Association, Inc


Figure 13.

Pathophysiological consequences of proposed abnormalities in arterial and cardiopulmonary baroreflex control in borderline hypertensive subjects. Impairment in arterial baroreflex inhibition of vasomotor centers would be expected to increase sympathetic activity and renin, but in supine position, augmentation of cardiopulmonary baroreflex inhibition of vasomotor center modulates expected increases in sympathetic activity and renin. With standing, however, decreases in cardiac filling pressure remove augmented cardiopulmonary baroreflex inhibition and permit impairment in arterial baroreceptor inhibition of vasomotor center to be expressed as augmented postural increases in sympathetic activity and renin.



Figure 14.

Hypothesized role of stimulation of left ventricular baroreceptors during exercise in patients with severe aortic stenosis. Top: afferent impulses originating in exercising leg muscles normally produce reflex vasoconstriction in nonexercising forearm. In patients with severe aortic stenosis, increases in left ventricular pressure activate left ventricular baroreceptors, which inhibit and reverse forearm vasoconstriction and may promote exertional syncope.

From Mark et al. 85, by copyright permission of The American Society for Clinical Investigation


Figure 15.

Forearm vascular responses to supine leg exercise in patient with severe calcific aortic stenosis before and after aortic valve replacement. Before operation (solid lines and dots) patient displayed abnormal forearm vasodilator response in leg exercise. After operation (dashed lines and circles) patient displayed normal forearm vasoconstrictor response to leg exercise.

From Mark et al. 85, by copyright permission of The American Society for Clinical Investigation
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Article Title: Cardiopulmonary Baroreflexes in Humans
 

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Allyn L. Mark, Giuseppe Mancia. Cardiopulmonary Baroreflexes in Humans. Compr Physiol 2011, Supplement 8: Handbook of Physiology, The Cardiovascular System, Peripheral Circulation and Organ Blood Flow: 795-813. First published in print 1983. doi: 10.1002/cphy.cp020321