Role of GABA and NO in the Paraventricular Nucleus-Mediated Reflex Inhibition of Renal Sympathetic Nerve Activity Following Stimulation of Right Atrial Receptors in the Rat

2003 ◽  
Vol 88 (3) ◽  
pp. 335-342 ◽  
Author(s):  
Zhuo Yang ◽  
John H. Coote
Keyword(s):  
Paraventricular Nucleus ◽  
Sympathetic Nerve Activity ◽  
Right Atrial ◽  
Reflex Inhibition ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Atrial Receptors ◽  
Renal Sympathetic ◽  
Stimulation Of

Interaction of vasopressin with area postrema during volume expansion

1987 ◽  
Vol 253 (4) ◽  
pp. R605-R610 ◽  
Author(s):  
E. M. Hasser ◽  
K. P. Undesser ◽  
V. S. Bishop
Keyword(s):  
Volume Expansion ◽  
Sympathetic Nerve Activity ◽  
Area Postrema ◽  
Right Atrial ◽  
Reflex Inhibition ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Maximum Inhibition ◽  
Renal Sympathetic

Effects of arginine vasopressin (AVP) on inhibition of renal sympathetic nerve activity (RSNA) during activation of cardiopulmonary reflexes by volume expansion were examined in conscious sinoaortic-denervated rabbits. The role of the area postrema in mediating these effects was also evaluated in rabbits subjected to area postrema lesion. Animals were subjected to 12% volume expansion with whole blood alone or during infusion of AVP (0.6 mU . kg-1 . min-1). Volume expansion in area postrema-intact animals caused a progressive reflex inhibition of RSNA (maximum = -36.5 +/- 3.3% delta RSNA). Vasopressin infusion did not significantly alter resting arterial pressure, right atrial pressure, heart rate, or RSNA. However, maximum inhibition of RSNA during volume expansion (-62.6 +/- 3.2% delta RSNA) was significantly augmented during AVP infusion, and the augmentation was reversed by a specific vascular (V1) AVP receptor antagonist. Vagotomy eliminated RSNA responses to volume expansion with or without AVP. In area postrema-lesioned animals, the RSNA response to volume expansion was similar to that of intact animals (-31.8 +/- 2.3% delta RSNA). However, AVP did not augment the RSNA response to volume expansion in lesioned animals (-30.4 +/- 2.5% delta RSNA). Thus exogenous AVP augmented cardiopulmonary reflex-mediated inhibition of RSNA due to volume expansion. This effect appeared to be mediated by the V1 AVP receptor and to require the presence of an intact area postrema.

Gestational effects on volume-sensitive cardiopulmonary receptor reflexes in the rat

1995 ◽  
Vol 268 (3) ◽  
pp. R736-R743 ◽  
Author(s):  
T. Hines ◽  
S. W. Mifflin
Keyword(s):  
Sympathetic Nerve Activity ◽  
Right Atrial ◽  
Nerve Activity ◽  
Pregnant Rats ◽  
Renal Sympathetic Nerve Activity ◽  
Cell Discharge ◽  
Afferent Stimulus ◽  
Gallamine Triethiodide ◽  
Renal Sympathetic ◽  
Stimulation Of

We tested the hypothesis that augmented reflex sympathoinhibition mediated by volume-sensitive cardiopulmonary (CP) receptors contributes to the vasodilation of pregnancy by comparing responses to acute volume expansion in 21-day-pregnant and age-matched virgin rats (n = 7) that were anesthetized (pentobarbital sodium, 50 mg/kg ip), paralyzed (gallamine triethiodide, 25 mg/kg iv), ventilated, and had undergone bilateral sinoaortic denervation. CP receptors were stimulated with intra-atrial injections of saline (50, 100, 200, and 300 microliter), and the following variables were recorded: 1) mean right atrial pressure (MRAP) to index the afferent stimulus intensity; 2) cell discharge in the nucleus tractus solitarii (NTS), the primary central terminus for CP afferents; and 3) mean arterial pressure (MAP), heart rate (HR), and renal sympathetic nerve activity (RSNA) to assess efferent reflex effects. Basal MAP was significantly lower in pregnant (71.5 +/- 3.8 mmHg) than in virgin rats (86.6 +/- 3.1 mmHg), and plasma volume was expanded in the pregnant group (17.6 +/- 1.1 vs. 10.0 +/- 0.7 ml, P < 0.05). Baseline MRAP was similar between groups. Saline injections evoked graded increases in MRAP, which were larger in gravid animals (P < 0.05). Volume injections evoked similar changes in NTS cell discharge between groups, but the responses were nongraded. Despite larger changes in MRAP in gravid rats, reflex effects on RSNA and HR were similar to those in control animals, and effects on MAP were attenuated in the pregnant group. We conclude that larger changes in MRAP in pregnant rats during stimulation of CP receptors are not associated with larger changes in central or efferent components of this reflex.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Role of the hypothalamic PVN in the regulation of renal sympathetic nerve activity and blood flow during hyperthermia and in heart failure

2010 ◽  
Vol 298 (4) ◽  
pp. F839-F846 ◽  
Author(s):  
Emilio Badoer
Keyword(s):  
Heart Failure ◽  
Blood Flow ◽  
Paraventricular Nucleus ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Renal Sympathetic

The hypothalamic paraventricular nucleus is a key integrative area in the brain involved in influencing sympathetic nerve activity and in the release of hormones or releasing factors that contribute to regulating body fluid homeostasis and endocrine function. The endocrine and hormonal regulatory function of the paraventricular nucleus is well studied, but the regulation of sympathetic nerve activity and blood flow by this region is less clear. Here we review the critical role of the paraventricular nucleus in regulating renal blood blow during hyperthermia and the evidence pointing to an important pathophysiological role of the paraventricular nucleus in the elevated renal sympathetic nerve activity that is a characteristic of heart failure.

Activation of 5-hydroxytryptamine-1A receptors suppresses cardiovascular responses evoked from the paraventricular nucleus

2011 ◽  
Vol 301 (4) ◽  
pp. R1088-R1097 ◽  
Author(s):  
Jouji Horiuchi ◽  
Alp Atik ◽  
Kamon Iigaya ◽  
Lachlan M. McDowall ◽  
Suzanne Killinger ◽  
...  
Keyword(s):  
Heart Rate ◽  
Paraventricular Nucleus ◽  
Sympathetic Nerve Activity ◽  
Cardiovascular Responses ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Dorsomedial Hypothalamus ◽  
Way 100635 ◽  
Renal Sympathetic ◽  
Stimulation Of

Activation of central 5-hydroxytryptamine-1A (5-HT1A) receptors powerfully inhibits stress-evoked cardiovascular responses mediated by the dorsomedial hypothalamus (DMH), as well as responses evoked by direct activation of neurons within the DMH. The hypothalamic paraventricular nucleus (PVN) also has a crucial role in cardiovascular regulation and is believed to regulate heart rate and renal sympathetic activity via pathways that are independent of the DMH. In this study, we determined whether cardiovascular responses evoked from the PVN are also modulated by activation of central 5-HT1A receptors. In anesthetized rats, the increases in heart rate and renal sympathetic nerve activity evoked by bicuculline injection into the PVN were greatly reduced (by 54% and 61%, respectively) by intravenous administration of (±)-8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT), an agonist of 5-HT1A receptors, but were then completely restored by subsequent administration of WAY-100635, a selective antagonist of 5-HT1A receptors. Microinjection of 8-OH-DPAT directly into the PVN did not significantly affect the responses to bicuculline injection into the PVN, nor did systemic administration of WAY-100635 alone. In control experiments, a large renal sympathoexcitatory response was evoked from both the PVN and DMH but not from the intermediate region in between; thus the evoked responses from the PVN were not due to activation of neurons in the DMH. The results indicate that activation of central 5-HT1A receptors located outside the PVN powerfully inhibits the tachycardia and renal sympathoexcitation evoked by stimulation of neurons in the PVN.

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

2018 ◽  
Vol 315 (5) ◽  
pp. H1368-H1382 ◽  
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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