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Cardiac Mechanoreceptors

Vernon S. Bishop, Alberto Malliani, Peter Thorén

10.1002/cphy.cp020315

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 Historical Landmarks
1.1 Depressor Reflexes From the Heart
1.2 Pressor Reflexes From the Heart
1.3 Electrophysiological Recordings From Vagal Afferents
1.4 Electrophysiological Recordings From Sympathetic Afferents
2 Morphological Notes
3 Receptors with Vagal Afferents
3.1 Atrial Receptors With Myelinated Afferents
3.2 Ventricular Receptors With Myelinated Afferents
3.3 Cardiac Receptors With Unmyelinated Afferents (C Fibers)
4 Tonic Vasomotor Inhibition from Cardiopulmonary Receptors
4.1 In Animals
4.2 In Humans
5 Role of Cardiopulmonary Reflexes
5.1 In Physiological State
5.2 In Pathophysiological State
6 Receptors with Sympathetic Afferents
6.1 Methodological Notes
6.2 Atrial Receptors
6.3 Ventricular Receptors
6.4 Coronary Receptors
6.5 Receptors in Large Thoracic Vessels
6.6 Reflex Effects
6.7 Positive‐Feedback Hypothesis
6.8 General Properties of Cardiovascular Sympathetic Afferents
7 Possible Interaction of Vagal and Sympathetic Afferents
8 Summary
Figure 1. Figure 1.

Recordings from A, B, and intermediate atrial receptors with myelinated vagal afferents in anesthetized cats.
Figure 2. Figure 2.

Effect of simultaneously distending middle and upper pulmonary vein‐atrial junctions and left atrial appendage. Top to bottom: respiratory pressure, end‐tidal CO2 pressure (PCO2), femoral artery blood pressure, heart rate, mean left atrial pressure, and electrocardiogram. Increase in heart rate during distension was 52 beats/min. Mean arterial pressure was the same throughout.

From Linden 244
Figure 3. Figure 3.

Impulse activity in right ventricular pressure receptor in dog. Pulmonary artery pressure was measured from lobar branch. A: control conditions; note marked respiratory variation. B: effect of tightening a snare around origin of pulmonary trunk. ECG, electrocardiogram; P, impulses from a vagal strip; t, time (50 Hz); R, tracheal pressure.

From Coleridge et al. 81
Figure 4. Figure 4.

Increase in right atrial C‐fiber discharge during stepwise increase in blood volume. Top to bottom: right atrial pressure, neurogram with corrected position of spikes within cardiac cycle, ECG, spike frequency, and change in blood volume. Receptor fired with cardiac rhythmicity at V wave (C and D), but A wave was markedly augmented as in post‐ectopic beat. D*: A wave.

From Thorén 420, by permission of the American Heart Association, Inc
Figure 5. Figure 5.

Relationship between activity in myelinated and unmyelinated vagal afferents from right and left atria of cats during increases in atrial pressure caused by graded occlusion of respective outflow tract. Each set of recordings is from single fiber.

From Thorén et al. 424, by permission of the American Heart Association, Inc
Figure 6. Figure 6.

Activity in single left ventricular C fiber plotted against left ventricular systolic and end‐diastolic pressures during graded aortic occlusion in control situation, during infusion of isoproterenol [Isuprel (1.25‐2.5 g/min)], and after administration of propranolol (0.2‐0.3 mg/kg). Values for maximal rate of increase in left ventricular pressure [(dP/dt)max] reflect changes in ventricular inotropism.

From Thorén 422
Figure 7. Figure 7.

Firing pattern in cardiac cycle of a left ventricular C fiber. A: control condition. B: after balloon occlusion of tricuspid valve. C: during brief aortic occlusion. D: after transfusion of 40 ml of dextran. E: during total conduction time of electrical stimulation over receptor area. Asterisk indicates corrected position of receptor activation in cardiac cycle after total conduction time as measured in E was taken into account. Receptor fired spontaneously in early systole. During aortic occlusion and transfusion, receptor discharged throughout systole. Occasional spikes in diastole are also seen in C.

From Thorén 421, by permission of the American Heart Association, Inc
Figure 8. Figure 8.

Effect of afferent stimulation of right cardiac nerve (4 V, 1 ms) on arterial blood pressure, heart rate, and gastric volume. Left panel: heart and blood pressure responses “escape” during continued stimulation, whereas gastric response is well maintained. Right panel: clear‐cut circulatory and gastric responses were obtained at stimulation frequencies as low as 1‐2 impulses/s. Maximal circulatory effects were obtained at 10 impulses/s, whereas the gastric response increased further with stimulation frequencies up to 40‐100 impulses.

From Abrahamsson and Thorén 8
Figure 9. Figure 9.

Pronounced hypotension, bradycardia, and gastric relaxation were produced by local application of nicotine to pericardium (left panel) and by intravenous injection of veratrum (right panel). Recovery of gastric volume after local administration of lidocaine in pericardium suggests that relaxation caused by veratrum was elicited from receptors localized in the heart.

From Thorén 428
Figure 10. Figure 10.

Changes (δ) in mean arterial pressure (MAP), heart rate (HR), cardiac output (MCO), and peripheral resistance (PR) from control (C) during bilateral vagal cold block (VB) in conscious dogs before (○) and after (•) sinoaortic denervation. *P < 0.05; ** P < 0.01; *** P < 0.001. Bars equal ± SEM.

From Bishop and Peterson 44, by permission of the American Heart Association, Inc
Figure 11. Figure 11.

Discharge frequency of left ventricular receptors from 7 cats plotted against time (logarithmic scale) after onset of occlusion of coronary artery supplying receptor area. Activity in 4 receptors was also observed after release of occlusion; in 3 of the 4 cats a rebound phenomenon occurred during first 2‐3 min after release

From Thorén 419
Figure 12. Figure 12.

Changes (δ) from control (C) in heart rate (HR), mean arterial pressure (MAP), cardiac output (MCO), and peripheral resistance (PR) to vagal cold block (VB) and subsequent coronary artery occlusion (VB + CO) in dogs with intact carotid sinuses. **P < 0.05; ***P < 0.001. Bracket shows changes from VB due to VB + CO. Bars equal ± SEM.

From Bishop and Peterson 44, by permission of the American Heart Association, Inc
Figure 13. Figure 13.

Changes (δ) in mean cardiac output (MCO), mean arterial pressure (MAP), mean left atrial pressure (MLAP), and peripheral resistance (PR) to coronary occlusion (CO), vagal block (VB), and vagal block plus coronary occlusion (VB + CO) in sinoaortic‐denervated dogs. P < 0.05; **P < 0.01; ***P < 0.001. P values for VB + CO refer to vagal block stage.

From Bishop and Peterson 44, by permission of the American Heart Association, Inc
Figure 14. Figure 14.

A: mean activity in left atrial C fibers plotted against mean left atrial pressure for 10 receptors in normotensive control rats (NCR) and 7 receptors in spontaneously hypertensive rats (SHR). Note that thresholds for C‐fiber endings in NCR were ∼5 mmHg. At pressures of 5‐12.5 mmHg there was a significant difference in discharge between the 2 groups of animals. *P < 0.05. B: relation between mean left atrial pressure and reflexly induced inhibition of renal sympathetic outflow for 6 NCR and 6 sinoaortic‐denervated SHR. Activity in renal nerves was inhibited at considerably higher pressure levels in SHR. **P < 0.001.

From Ricksten et al. 363
Figure 15. Figure 15.

Activity of a fiber with left atrial endings. Tracings in each chart from top to bottom: endotracheal pressure (inflation upward), arterial blood pressure, right atrial pressure, ECG, and neural activity. A: control. B: injection, starting at arrow, of 2 ml warm saline. C: constriction of the thoracic aorta (marked by bar). D: beginning of rise in arterial blood pressure produced by intravenous injection of 3 μg norepinephrine. E: mechanical probing of area of left atrium in the beating heart. F: electrical stimulation of left inferior cardiac nerve activating the afferent fiber. First biphasic deflection is artifact of the stimulus, whereas second upward and smaller deflection is action potential of the fiber. Fiber length was ∼7 cm; its conduction velocity was 32 m/s.

From Malliani et al. 274
Figure 16. Figure 16.

Activity of a fiber with left ventricular endings. Tracings in each chart from top to bottom: endotracheal pressure (inflation upward), arterial blood pressure, right atrial pressure, ECG, and neural activity. A: spontaneous activity. B: abolition of discharge obtained by constriction of the pulmonary artery (marked by bar). C: mechanical probing of area of left ventricle in the beating heart. D: repetition of probing surface of ventricular wall at end of experiment in opened, nonbeating heart.

From Malliani et al. 268
Figure 17. Figure 17.

Effects of various experimental interventions on impulse activity. AO, aortic occlusion; Isopr., intravenous injection of isoproterenol; Inf., intravenous infusion of isotonic solution; LCO, left coronary occlusion; IVCO, inferior vena cava occlusion; Bleed., bleeding; ACh., intravenous injection of acetylcholine; Asph., asphyxia; VF, ventricular fibrillation; n, number of fibers studied; ***P < 0.001; **P < 0.02; NS, not statistically significant. Bars equal ± SEM.

From Casati et al. 68
Figure 18. Figure 18.

Activity of an unmyelinated afferent sympathetic nerve fiber with its receptive field in the left ventricle. Tracings in each chart from top to bottom: ECG, systemic arterial pressure, right atrial pressure, neural activity. (All tracings are cathode‐ray oscilloscope recordings.) A: occlusion of descending thoracic aorta (indicated by rise in arterial pressure). B: intravenous injection of 5 ml warm saline, beginning at arrow. C: occlusion of inferior vena cava, released at arrow. D: electrical stimulation of left inferior cardiac nerve activating the afferent fiber. First biphasic deflection is artifact of the stimulus, detectable also on ECG, whereas second biphasic deflection is action potential of the fiber. Fiber length was ∼3.8 cm; its conduction velocity was 0.92 m/s. E: mechanical probing of area of external surface of left ventricle (marked by bar) in the nonbeating heart after bleeding the animal to death. Note afterdischarge, which is typical of C fibers.

From Casati et al. 68
Figure 19. Figure 19.

Effects of ventricular fibrillation on activity of 2 nerve filaments. Tracings in each chart from top to bottom: ECG, systemic arterial pressure, right atrial pressure, neural activity. (All tracings are cathode‐ray oscilloscope recordings.) A: nerve filament impulses from 2 unmyelinated fibers. Fiber yielding biphasic action potentials had its receptive field in the depth of the left ventricle and a conduction velocity of 0.32 m/s; fiber producing monophasic potentials had its receptive field in the left atrium and a conduction velocity of 0.53 m/s. A (upper): episode of ventricular fibrillation induced by gentle mechanical stimulation of right ventricle, corresponding to ectopic beat, preceding the episode itself by a few cardiac cycles. A (lower): spontaneous return of ventricles to normal action after −8.0 s. B: nerve filament impulses of an unmyelinated and a myelinated afferent fiber, each with its receptive field in left ventricle. Potentials of unmyelinated fiber (conduction velocity, 0.36 m/s) are marked with dots. Highest potentials were produced by myelinated fiber (conduction velocity, 7.23 m/s). B (upper): ventricular fibrillation induced by high‐frequency electrical stimulation of right ventricle. B (lower): spontaneous return of ventricles to normal action after 6.8 s.

From Casati et al. 68
Figure 20. Figure 20.

Activity of an unmyelinated afferent sympathetic nerve fiber with a left ventricular sensory field. Tracings in each chart from top to bottom: systemic arterial pressure, coronary perfusion pressure, and neural impulse activity (cathode‐ray oscilloscope recordings). A: interruption of left main coronary artery perfusion. B: intracoronary administration, beginning at arrow, of bradykinin, 5 ng/kg. C: intracoronary administration of bradykinin, 10 ng/kg. D: intracoronary administration of bradykinin, 30 ng/kg. E: electrical stimulation of left inferior cardiac nerve activating the afferent fiber. First biphasic deflection is artifact of the stimulus, and second biphasic deflection is action potential of the fiber. Fiber length was ∼8 cm; its conduction velocity was 0.45 m/s. F: mechanical probing (marked by bar) of area of external surface of left ventricle. Note afterdischarge, which is typical of unmyelinated afferents.

From Lombardi et al. 257, by permission of the American Heart Association, Inc
Figure 21. Figure 21.

Activity of an unmyelinated afferent sympathetic nerve fiber (C fiber) with receptive field in distal third of aortic arch. A: control. B: occlusion of descending aorta. C, D, E, F, H, and I: effects of stretching aortic wall by distending a latex balloon in distal part of aortic arch. Top tracing, pressure applied to distending balloon; bottom tracing, neural activity. G: electrical stimulation of left inferior cardiac nerve activating the fiber. Fiber length was ∼5 cm; its conduction velocity was 1 m/s. Tracings in A and B from top to bottom: endotracheal pressure (inflation upward), aortic and femoral artery pressures, ECG, and neural activity.

From Malliani and Pagani 269
Figure 22. Figure 22.

Effects of intravenous infusion of Locke solution and bleeding on impulse activity of a single afferent fiber innervating a pulmonary artery receptor. Charts are continuous records. Tracings in each chart from top to bottom: impulse activity, pulmonary artery pressure (PAP), and ECG. Intravenous infusion of Locke solution (15 ml) in C at arrow.

From Nishi et al. 309
Figure 23. Figure 23.

Activity of a single afferent sympathetic fiber innervating left middle pulmonary vein. Tracings in each chart from top to bottom: systemic blood pressure, right atrial pressure, left atrial pressure, ECG, and neural activity. A: control. B: 10 s after beginning of intravenous infusion of saline. C: end of infusion (100 ml infused in ∼5 min).

From Lombardi et al. 258
Figure 24. Figure 24.

Effects of progressively increasing aortic stretch on arterial pressure and heart rate in a conscious dog. Distending balloon pressure, obviously not corresponding to pressure effectively applied to aortic walls, is displayed in bottom tracing as index of progressive stretch.

From Malliani et al. 270
Figure 25. Figure 25.

Suggested mechanisms underlying neural control of arterial blood pressure. Baroreceptors are indicated as example of receptors that activate negative‐feedback mechanisms. Coexistence of inhibitory components in excitatory reflexes mediated by sympathetic afferents is represented by broken line. CNS, central nervous system; CV, cardiovascular.

From Malliani et al. 270


Figure 1.

Recordings from A, B, and intermediate atrial receptors with myelinated vagal afferents in anesthetized cats.



Figure 2.

Effect of simultaneously distending middle and upper pulmonary vein‐atrial junctions and left atrial appendage. Top to bottom: respiratory pressure, end‐tidal CO2 pressure (PCO2), femoral artery blood pressure, heart rate, mean left atrial pressure, and electrocardiogram. Increase in heart rate during distension was 52 beats/min. Mean arterial pressure was the same throughout.

From Linden 244


Figure 3.

Impulse activity in right ventricular pressure receptor in dog. Pulmonary artery pressure was measured from lobar branch. A: control conditions; note marked respiratory variation. B: effect of tightening a snare around origin of pulmonary trunk. ECG, electrocardiogram; P, impulses from a vagal strip; t, time (50 Hz); R, tracheal pressure.

From Coleridge et al. 81


Figure 4.

Increase in right atrial C‐fiber discharge during stepwise increase in blood volume. Top to bottom: right atrial pressure, neurogram with corrected position of spikes within cardiac cycle, ECG, spike frequency, and change in blood volume. Receptor fired with cardiac rhythmicity at V wave (C and D), but A wave was markedly augmented as in post‐ectopic beat. D*: A wave.

From Thorén 420, by permission of the American Heart Association, Inc


Figure 5.

Relationship between activity in myelinated and unmyelinated vagal afferents from right and left atria of cats during increases in atrial pressure caused by graded occlusion of respective outflow tract. Each set of recordings is from single fiber.

From Thorén et al. 424, by permission of the American Heart Association, Inc


Figure 6.

Activity in single left ventricular C fiber plotted against left ventricular systolic and end‐diastolic pressures during graded aortic occlusion in control situation, during infusion of isoproterenol [Isuprel (1.25‐2.5 g/min)], and after administration of propranolol (0.2‐0.3 mg/kg). Values for maximal rate of increase in left ventricular pressure [(dP/dt)max] reflect changes in ventricular inotropism.

From Thorén 422


Figure 7.

Firing pattern in cardiac cycle of a left ventricular C fiber. A: control condition. B: after balloon occlusion of tricuspid valve. C: during brief aortic occlusion. D: after transfusion of 40 ml of dextran. E: during total conduction time of electrical stimulation over receptor area. Asterisk indicates corrected position of receptor activation in cardiac cycle after total conduction time as measured in E was taken into account. Receptor fired spontaneously in early systole. During aortic occlusion and transfusion, receptor discharged throughout systole. Occasional spikes in diastole are also seen in C.

From Thorén 421, by permission of the American Heart Association, Inc


Figure 8.

Effect of afferent stimulation of right cardiac nerve (4 V, 1 ms) on arterial blood pressure, heart rate, and gastric volume. Left panel: heart and blood pressure responses “escape” during continued stimulation, whereas gastric response is well maintained. Right panel: clear‐cut circulatory and gastric responses were obtained at stimulation frequencies as low as 1‐2 impulses/s. Maximal circulatory effects were obtained at 10 impulses/s, whereas the gastric response increased further with stimulation frequencies up to 40‐100 impulses.

From Abrahamsson and Thorén 8


Figure 9.

Pronounced hypotension, bradycardia, and gastric relaxation were produced by local application of nicotine to pericardium (left panel) and by intravenous injection of veratrum (right panel). Recovery of gastric volume after local administration of lidocaine in pericardium suggests that relaxation caused by veratrum was elicited from receptors localized in the heart.

From Thorén 428


Figure 10.

Changes (δ) in mean arterial pressure (MAP), heart rate (HR), cardiac output (MCO), and peripheral resistance (PR) from control (C) during bilateral vagal cold block (VB) in conscious dogs before (○) and after (•) sinoaortic denervation. *P < 0.05; ** P < 0.01; *** P < 0.001. Bars equal ± SEM.

From Bishop and Peterson 44, by permission of the American Heart Association, Inc


Figure 11.

Discharge frequency of left ventricular receptors from 7 cats plotted against time (logarithmic scale) after onset of occlusion of coronary artery supplying receptor area. Activity in 4 receptors was also observed after release of occlusion; in 3 of the 4 cats a rebound phenomenon occurred during first 2‐3 min after release

From Thorén 419


Figure 12.

Changes (δ) from control (C) in heart rate (HR), mean arterial pressure (MAP), cardiac output (MCO), and peripheral resistance (PR) to vagal cold block (VB) and subsequent coronary artery occlusion (VB + CO) in dogs with intact carotid sinuses. **P < 0.05; ***P < 0.001. Bracket shows changes from VB due to VB + CO. Bars equal ± SEM.

From Bishop and Peterson 44, by permission of the American Heart Association, Inc


Figure 13.

Changes (δ) in mean cardiac output (MCO), mean arterial pressure (MAP), mean left atrial pressure (MLAP), and peripheral resistance (PR) to coronary occlusion (CO), vagal block (VB), and vagal block plus coronary occlusion (VB + CO) in sinoaortic‐denervated dogs. P < 0.05; **P < 0.01; ***P < 0.001. P values for VB + CO refer to vagal block stage.

From Bishop and Peterson 44, by permission of the American Heart Association, Inc


Figure 14.

A: mean activity in left atrial C fibers plotted against mean left atrial pressure for 10 receptors in normotensive control rats (NCR) and 7 receptors in spontaneously hypertensive rats (SHR). Note that thresholds for C‐fiber endings in NCR were ∼5 mmHg. At pressures of 5‐12.5 mmHg there was a significant difference in discharge between the 2 groups of animals. *P < 0.05. B: relation between mean left atrial pressure and reflexly induced inhibition of renal sympathetic outflow for 6 NCR and 6 sinoaortic‐denervated SHR. Activity in renal nerves was inhibited at considerably higher pressure levels in SHR. **P < 0.001.

From Ricksten et al. 363


Figure 15.

Activity of a fiber with left atrial endings. Tracings in each chart from top to bottom: endotracheal pressure (inflation upward), arterial blood pressure, right atrial pressure, ECG, and neural activity. A: control. B: injection, starting at arrow, of 2 ml warm saline. C: constriction of the thoracic aorta (marked by bar). D: beginning of rise in arterial blood pressure produced by intravenous injection of 3 μg norepinephrine. E: mechanical probing of area of left atrium in the beating heart. F: electrical stimulation of left inferior cardiac nerve activating the afferent fiber. First biphasic deflection is artifact of the stimulus, whereas second upward and smaller deflection is action potential of the fiber. Fiber length was ∼7 cm; its conduction velocity was 32 m/s.

From Malliani et al. 274


Figure 16.

Activity of a fiber with left ventricular endings. Tracings in each chart from top to bottom: endotracheal pressure (inflation upward), arterial blood pressure, right atrial pressure, ECG, and neural activity. A: spontaneous activity. B: abolition of discharge obtained by constriction of the pulmonary artery (marked by bar). C: mechanical probing of area of left ventricle in the beating heart. D: repetition of probing surface of ventricular wall at end of experiment in opened, nonbeating heart.

From Malliani et al. 268


Figure 17.

Effects of various experimental interventions on impulse activity. AO, aortic occlusion; Isopr., intravenous injection of isoproterenol; Inf., intravenous infusion of isotonic solution; LCO, left coronary occlusion; IVCO, inferior vena cava occlusion; Bleed., bleeding; ACh., intravenous injection of acetylcholine; Asph., asphyxia; VF, ventricular fibrillation; n, number of fibers studied; ***P < 0.001; **P < 0.02; NS, not statistically significant. Bars equal ± SEM.

From Casati et al. 68


Figure 18.

Activity of an unmyelinated afferent sympathetic nerve fiber with its receptive field in the left ventricle. Tracings in each chart from top to bottom: ECG, systemic arterial pressure, right atrial pressure, neural activity. (All tracings are cathode‐ray oscilloscope recordings.) A: occlusion of descending thoracic aorta (indicated by rise in arterial pressure). B: intravenous injection of 5 ml warm saline, beginning at arrow. C: occlusion of inferior vena cava, released at arrow. D: electrical stimulation of left inferior cardiac nerve activating the afferent fiber. First biphasic deflection is artifact of the stimulus, detectable also on ECG, whereas second biphasic deflection is action potential of the fiber. Fiber length was ∼3.8 cm; its conduction velocity was 0.92 m/s. E: mechanical probing of area of external surface of left ventricle (marked by bar) in the nonbeating heart after bleeding the animal to death. Note afterdischarge, which is typical of C fibers.

From Casati et al. 68


Figure 19.

Effects of ventricular fibrillation on activity of 2 nerve filaments. Tracings in each chart from top to bottom: ECG, systemic arterial pressure, right atrial pressure, neural activity. (All tracings are cathode‐ray oscilloscope recordings.) A: nerve filament impulses from 2 unmyelinated fibers. Fiber yielding biphasic action potentials had its receptive field in the depth of the left ventricle and a conduction velocity of 0.32 m/s; fiber producing monophasic potentials had its receptive field in the left atrium and a conduction velocity of 0.53 m/s. A (upper): episode of ventricular fibrillation induced by gentle mechanical stimulation of right ventricle, corresponding to ectopic beat, preceding the episode itself by a few cardiac cycles. A (lower): spontaneous return of ventricles to normal action after −8.0 s. B: nerve filament impulses of an unmyelinated and a myelinated afferent fiber, each with its receptive field in left ventricle. Potentials of unmyelinated fiber (conduction velocity, 0.36 m/s) are marked with dots. Highest potentials were produced by myelinated fiber (conduction velocity, 7.23 m/s). B (upper): ventricular fibrillation induced by high‐frequency electrical stimulation of right ventricle. B (lower): spontaneous return of ventricles to normal action after 6.8 s.

From Casati et al. 68


Figure 20.

Activity of an unmyelinated afferent sympathetic nerve fiber with a left ventricular sensory field. Tracings in each chart from top to bottom: systemic arterial pressure, coronary perfusion pressure, and neural impulse activity (cathode‐ray oscilloscope recordings). A: interruption of left main coronary artery perfusion. B: intracoronary administration, beginning at arrow, of bradykinin, 5 ng/kg. C: intracoronary administration of bradykinin, 10 ng/kg. D: intracoronary administration of bradykinin, 30 ng/kg. E: electrical stimulation of left inferior cardiac nerve activating the afferent fiber. First biphasic deflection is artifact of the stimulus, and second biphasic deflection is action potential of the fiber. Fiber length was ∼8 cm; its conduction velocity was 0.45 m/s. F: mechanical probing (marked by bar) of area of external surface of left ventricle. Note afterdischarge, which is typical of unmyelinated afferents.

From Lombardi et al. 257, by permission of the American Heart Association, Inc


Figure 21.

Activity of an unmyelinated afferent sympathetic nerve fiber (C fiber) with receptive field in distal third of aortic arch. A: control. B: occlusion of descending aorta. C, D, E, F, H, and I: effects of stretching aortic wall by distending a latex balloon in distal part of aortic arch. Top tracing, pressure applied to distending balloon; bottom tracing, neural activity. G: electrical stimulation of left inferior cardiac nerve activating the fiber. Fiber length was ∼5 cm; its conduction velocity was 1 m/s. Tracings in A and B from top to bottom: endotracheal pressure (inflation upward), aortic and femoral artery pressures, ECG, and neural activity.

From Malliani and Pagani 269


Figure 22.

Effects of intravenous infusion of Locke solution and bleeding on impulse activity of a single afferent fiber innervating a pulmonary artery receptor. Charts are continuous records. Tracings in each chart from top to bottom: impulse activity, pulmonary artery pressure (PAP), and ECG. Intravenous infusion of Locke solution (15 ml) in C at arrow.

From Nishi et al. 309


Figure 23.

Activity of a single afferent sympathetic fiber innervating left middle pulmonary vein. Tracings in each chart from top to bottom: systemic blood pressure, right atrial pressure, left atrial pressure, ECG, and neural activity. A: control. B: 10 s after beginning of intravenous infusion of saline. C: end of infusion (100 ml infused in ∼5 min).

From Lombardi et al. 258


Figure 24.

Effects of progressively increasing aortic stretch on arterial pressure and heart rate in a conscious dog. Distending balloon pressure, obviously not corresponding to pressure effectively applied to aortic walls, is displayed in bottom tracing as index of progressive stretch.

From Malliani et al. 270


Figure 25.

Suggested mechanisms underlying neural control of arterial blood pressure. Baroreceptors are indicated as example of receptors that activate negative‐feedback mechanisms. Coexistence of inhibitory components in excitatory reflexes mediated by sympathetic afferents is represented by broken line. CNS, central nervous system; CV, cardiovascular.

From Malliani et al. 270
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Article Title: Cardiac Mechanoreceptors
 

How to Cite

Vernon S. Bishop, Alberto Malliani, Peter Thorén. Cardiac Mechanoreceptors. Compr Physiol 2011, Supplement 8: Handbook of Physiology, The Cardiovascular System, Peripheral Circulation and Organ Blood Flow: 497-555. First published in print 1983. doi: 10.1002/cphy.cp020315