Cardiac receptors modulate the renal sympathetic response to dynamic exercise in rabbits

Activation of cardiac sensory receptors with vagal afferents can result in inhibition of sympathetic outflow to the peripheral circulation. This study investigated whether the regulation of renal sympathetic nerve activity (RSNA) during dynamic exercise was modulated by cardiac sensory receptors. RSNA, blood pressure, and heart rate were measured in seven New Zealand White rabbits during treadmill exercise while cardiac receptors were intact (saline), during cardiac neural block with 2% procaine (2% PCN), and during cardiac efferent receptor block with methscopolamine and atenolol (M + A). Drugs were infused into the pericardial space via a chronic catheter. Two exercise protocols were used: 7 m/min (5 min) and 12 m/min (2 min) at 0% grade. The increases in HR during exercise at 7 and 12 m/min were attenuated with 2% PCN or M + A. At 12 m/min, blood pressure was significantly lower with 2% PCN (76 +/- 4 mmHg) or M + A (76 +/- 3 mmHg) than with saline (86 +/- 2 mmHg). Abolition of cardiac afferent input with 2% PCN resulted in a potentiated RSNA response to exercise at 7 m/min (+134 +/- 37%) and 12 m/min (+234 +/- 45%) relative to saline (+62 +/- 24 and +101 +/- 28%) or M + A (+19 +/- 9 and +52 +/- 19%, P < 0.05). These results suggest that cardiac sensory receptors attenuate sympathetic drive to the kidney during dynamic exercise in conscious rabbits.

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Effects of combined histamine H1 and H2 receptor blockade on hemodynamic responses to dynamic exercise in males with high-normal blood pressure

Applied Physiology Nutrition and Metabolism ◽

10.1139/apnm-2019-0645 ◽

2020 ◽

Vol 45 (7) ◽

pp. 769-776

Author(s):

Ashley Naylor ◽

Brian Shariffi ◽

Trevor L. Gillum ◽

Boyer William ◽

Sean Sullivan ◽

...

Keyword(s):

Blood Pressure ◽

Dynamic Exercise ◽

Histamine Receptors ◽

Normal Group ◽

Receptor Blockade ◽

Peripheral Vasoconstriction ◽

Before And After ◽

Group A ◽

Postexercise Hypotension ◽

Response To Exercise

While postexercise hypotension is associated with histamine H1 and H2 receptor-mediated postexercise vasodilation, effects of histaminergic vasodilation on blood pressure (BP) in response to dynamic exercise are not known. Thus, in 20 recreationally active male participants (10 normotensive and 10 with high-normal BP) we examined the effects of histamine H1 and H2 receptor blockade on cardiac output (CO), mean atrial pressure (MAP), aortic stiffness (AoStiff), and total vascular conductance (TVC) at rest and during progressive cycling exercise. Compared with the normotensive group, MAP, CO, and AoStiff were higher in the high-normal group before and after the blockade at rest, while TVC was similar. At the 40% workload, the blockade significantly increased MAP in both groups, while no difference was found in the TVC. CO was higher in the high-normal group than the normotensive group in both conditions. At the 60% workload, the blockade substantially increased MAP and decreased TVC in the normotensive group, while there were no changes in the high-normal group. A similar CO response pattern was observed at the 60% workload. These findings suggest that the mechanism eliciting an exaggerated BP response to exercise in the high-normal group may be partially due to the inability of histamine receptors. Novelty Males with high-normal BP had an exaggerated BP response to exercise. The overactive BP response is known due to an increase in peripheral vasoconstriction. Increase in peripheral vasoconstriction is partially due to inability of histamine receptors.

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Mechano- and chemoreceptor modulation of renal sympathetic nerve activity at birth in fetal sheep

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1999.276.5.r1295 ◽

1999 ◽

Vol 276 (5) ◽

pp. R1295-R1301 ◽

Cited By ~ 2

Author(s):

Jeffrey L. Segar ◽

Oliva J. Smith ◽

Aaron T. Holley

Keyword(s):

Blood Pressure ◽

Cesarean Section ◽

Sympathetic Nerve ◽

Sympathetic Nerve Activity ◽

Afferent Input ◽

Ang Ii ◽

Nerve Activity ◽

Renal Sympathetic Nerve Activity ◽

Renal Sympathetic Nerve ◽

Renal Sympathetic

Physiological responses at birth include increases in heart rate (HR), blood pressure, sympathetic nerve activity, and circulating vasoactive peptides. The factors mediating these responses are not known. To test the hypothesis that afferent input from peripheral mechanoreceptors (arterial and cardiopulmonary baroreceptors) and chemoreceptors contribute to the sympathoexcitatory and hormonal responses at birth, we studied the effects of sinoaortic denervation (SAD) and SAD with vagotomy (Vx) on changes in HR, mean arterial blood pressure (MABP), renal sympathetic nerve activity (RSNA), and catecholamine, arginine vasopressin (AVP), and ANG II levels at birth in term sheep. One hour after delivery by cesarean section, RSNA increased by 168 ± 49 and 192 ± 32% (relative to fetal values) in SAD and SAD-Vx animals, respectively. Significant increases in HR (18 ± 5 and 20 ± 6%) and MABP (24 ± 4 and 20 ± 5%) were also observed 1 h after delivery in SAD and SAD-Vx lambs, respectively. These responses are similar to those seen in intact sheep delivered at the same gestational age. AVP levels markedly increased after birth (19.8 ± 6.7 to 136.1 ± 75.9 pg/ml) in SAD-Vx lambs, whereas SAD animals displayed no change in AVP concentrations. Plasma ANG II also did not change after birth in either group, although levels were consistently higher ( P < 0.01) in SAD compared with SAD-Vx animals. In the presence of SAD, Vx resulted in significantly greater plasma levels of norepinephrine, although levels did not change after birth in either group. The epinephrine responses at birth were similar in both groups of animals. The present data suggest that afferent input from peripheral chemoreceptors and mechanoreceptors contributes little to the hemodynamic and sympathetic responses after delivery by cesarean section. On the other hand, these peripheral mechanisms appear to be involved in modulating endocrine responses at birth.

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Acetylstrophanthidin-induced reflex inhibition of canine renal sympathetic nerve activity mediated by cardiac receptors with vagal afferents.

Circulation Research ◽

10.1161/01.res.44.1.8 ◽

1979 ◽

Vol 44 (1) ◽

pp. 8-15 ◽

Cited By ~ 50

Author(s):

M D Thames

Keyword(s):

Sympathetic Nerve ◽

Sympathetic Nerve Activity ◽

Vagal Afferents ◽

Reflex Inhibition ◽

Nerve Activity ◽

Renal Sympathetic Nerve Activity ◽

Renal Sympathetic Nerve ◽

Cardiac Receptors ◽

Renal Sympathetic

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Effects of intraduodenal injection of Lactobacillus johnsonii La1 on renal sympathetic nerve activity and blood pressure in urethane-anesthetized rats

Neuroscience Letters ◽

10.1016/j.neulet.2005.07.036 ◽

2005 ◽

Vol 389 (2) ◽

pp. 109-114 ◽

Cited By ~ 90

Author(s):

Mamoru Tanida ◽

Toshihiko Yamano ◽

Keiko Maeda ◽

Nobuaki Okumura ◽

Yoichi Fukushima ◽

...

Keyword(s):

Blood Pressure ◽

Sympathetic Nerve ◽

Sympathetic Nerve Activity ◽

Lactobacillus Johnsonii ◽

Nerve Activity ◽

Renal Sympathetic Nerve Activity ◽

Renal Sympathetic Nerve ◽

Anesthetized Rats ◽

Renal Sympathetic

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Chemical stimulation of the locus coeruleus: inhibitory effects on blood pressure, heart rate and renal sympathetic nerve activity

Journal of the Autonomic Nervous System ◽

10.1016/0165-1838(92)90064-n ◽

1992 ◽

Vol 41 (3) ◽

pp. 231

Author(s):

Takashi Miyawaki ◽

Hiroshi Kawamura ◽

Michinobu Hatano

Keyword(s):

Blood Pressure ◽

Heart Rate ◽

Sympathetic Nerve ◽

Sympathetic Nerve Activity ◽

Chemical Stimulation ◽

Inhibitory Effects ◽

Nerve Activity ◽

Renal Sympathetic Nerve Activity ◽

Renal Sympathetic ◽

Stimulation Of

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Role of the heart in blood pressure lowering during chronic baroreflex activation: insight from an in silico analysis

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00302.2018 ◽

2018 ◽

Vol 315 (5) ◽

pp. H1368-H1382 ◽

Cited By ~ 3

Author(s):

John S. Clemmer ◽

W. Andrew Pruett ◽

Robert L. Hester ◽

Radu Iliescu ◽

Thomas E. Lohmeier

Keyword(s):

Blood Pressure ◽

Mathematical Model ◽

Renal Denervation ◽

Sympathetic Nerve Activity ◽

Blood Pressure Lowering ◽

Nerve Activity ◽

Renal Sympathetic Nerve Activity ◽

Pressure Lowering ◽

Renal Sympathetic ◽

Stimulation Of

Electrical stimulation of the baroreflex chronically suppresses sympathetic activity and arterial pressure and is currently being evaluated for the treatment of resistant hypertension. The antihypertensive effects of baroreflex activation are often attributed to renal sympathoinhibition. However, baroreflex activation also decreases heart rate, and robust blood pressure lowering occurs even after renal denervation. Because controlling renal sympathetic nerve activity (RSNA) and cardiac autonomic activity cannot be achieved experimentally, we used an established mathematical model of human physiology (HumMod) to provide mechanistic insights into their relative and combined contributions to the cardiovascular responses during baroreflex activation. Three-week responses to baroreflex activation closely mimicked experimental observations in dogs including decreases in blood pressure, heart rate, and plasma norepinephrine and increases in plasma atrial natriuretic peptide (ANP), providing validation of the model. Simulations showed that baroreflex-induced alterations in cardiac sympathetic and parasympathetic activity lead to a sustained depression of cardiac function and increased secretion of ANP. Increased ANP and suppression of RSNA both enhanced renal excretory function and accounted for most of the chronic blood pressure lowering during baroreflex activation. However, when suppression of RSNA was blocked, the blood pressure response to baroreflex activation was not appreciably impaired due to inordinate fluid accumulation and further increases in atrial pressure and ANP secretion. These simulations provide a mechanistic understanding of experimental and clinical observations showing that baroreflex activation effectively lowers blood pressure in subjects with previous renal denervation. NEW & NOTEWORTHY Both experimental and clinical studies have shown that the presence of renal nerves is not an obligate requirement for sustained reductions in blood pressure during chronic electrical stimulation of the carotid baroreflex. Simulations using HumMod, a mathematical model of integrative human physiology, indicated that both increased secretion of atrial natriuretic peptide and suppressed renal sympathetic nerve activity play key roles in mediating long-term reductions in blood pressure during chronic baroreflex activation.

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