Paraventricular nucleus is involved in the central pathway of cardiac sympathetic afferent reflex in rats

Zhong, Ming-Kui; Duan, Yang-Can; Chen, Aidong; Xu, Bo; Gao, Xing-Ya; De, Wei; Zhu, Guo‐Qing

doi:10.1113/expphysiol.2007.041632

Cited by 65 publications

(68 citation statements)

References 46 publications

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“…51 Lesions in the VMH and PVN increase food intake and decrease sympathetic activity, whereas lesions in the LH decrease food intake and increase sympathetic activity. [52][53][54][55][56] Thus, the SNS activity is controlled in a similar manner in VMH and PVN, which clearly differs from LH. The SNS activity is relayed to the periphery via noradrenalin that binds b-adrenoreceptors, and in vitro studies showed that b-receptor agonists decreased leptin secretion by adipocytes.…”

Section: Effects On Body Composition and Endocrine Parametersmentioning

confidence: 99%

Melanocortin receptor-mediated effects on obesity are distributed over specific hypothalamic regions

et al. 2010

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Objective: Reduction of melanocortin signaling in the brain results in obesity. However, where in the brain reduced melanocortin signaling mediates this effect is poorly understood. Design: We determined the effects of long-term inhibition of melanocortin receptor activity in specific brain regions of the rat brain. Melanocortin signaling was inhibited by injection of a recombinant adeno-associated viral (rAAV) vector that overexpressed Agouti-related peptide (AgRP) into the paraventricular nucleus (PVN), the ventromedial hypothalamus (VMH), the lateral hypothalamus (LH) or the accumbens shell (Acc). Results: Overexpression of AgRP in the rat PVN, VMH or LH increased bodyweight, the percentage of white adipose tissue, plasma leptin and insulin concentrations and food intake. Food intake was mainly increased because of an increase in meal size in the light and dark phases, after overexpression of AgRP in the PVN, LH or VMH. Overexpression of AgRP in the PVN or VMH reduced average body core temperature in the dark on day 40 post injection, whereas AgRP overexpression in the LH did not affect temperature. In addition, overexpression of AgRP in the PVN, LH or VMH did not significantly alter mRNA expression of AgRP, neuropeptide Y (NPY), pro-opiomelanocortin (POMC) or suppressor of cytokine signaling 3 (SOCS3) in the arcuate. Overexpression of AgRP in the Acc did not have any effect on the measured parameters. Conclusions: Reduction of melanocortin signaling in several hypothalamic regions increased meal size. However, there were brain area-specific effects on other parameters such as core temperature and plasma leptin concentrations. In a previous study, where NPY was overexpressed with an rAAV vector in the PVN and LH, meal frequency and meal size were increased respectively, whereas locomotor activity was reduced by NPY overexpression at both nuclei. Taken together, AgRP and NPY have complementary roles in energy balance.

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Section: Effects On Body Composition and Endocrine Parametersmentioning

confidence: 99%

Melanocortin receptor-mediated effects on obesity are distributed over specific hypothalamic regions

et al. 2010

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“…PVN is an important integrative site in the control of ejaculatory reflexes, and it is also a main center in regulating the sympathetic outflow via its projections to the intermediolateral column of the spinal cord (Marson & McKenna, 1994;Zhong et al, 2008). Based on the regulation activity of N-methyl-Daspartic acid (NMDA) receptors in PVN on the sympathetic nerve discharges (Li et al, 2001), we hypothesized that NMDA receptors in PVN could centrally mediate ejaculatory responses through affecting the sympathetic outflow.…”

Section: Introductionmentioning

confidence: 99%

Centrally mediated ejaculatory response via sympathetic outflow in rats: role of N‐methyl‐D‐aspartic acid receptors in paraventricular nucleus

et al. 2016

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SUMMARYEjaculation is mediated by a spinal generator, which integrates inputs related to the sexual activity and coordinates sympathetic, parasympathetic, and motor outflow. Previous clinical studies indicate that primary premature ejaculation is related to the hyperactivity of the sympathetic nervous system. In this study, we explored the roles of N-methyl-D-aspartic acid (NMDA) receptors in paraventricular nucleus of the hypothalamus (PVN) on ejaculatory responses and its potential mechanism in the rats. We found that microinjection of 0.20 nmol NMDA into the PVN reduced the latency of intromission and facilitated ejaculation during copulation. Moreover, delayed ejaculation and intromission were observed after the rats were microinjected with NMDA receptor antagonist D (À)-2-Amino-5-phosphonopentanoic acid (AP-5). However, we discovered that microinjection of NMDA into PVN significantly increased baseline lumbar splanchnic nerve activity (LSNA), and the NMDA dose was positively correlated with the increased LSNA (r = 0.875, p = 0.04). Meanwhile, the plasma norepinephrine level in rats injected with NMDA was much higher than that in rats injected with saline (1453.4 AE 136.4 pg/mL vs. 492.3 AE 36.8 pg/mL, p < 0.01). Additionally, AP-5 reduced the baseline LSNA and abrogated the enhancing activity of NMDA in LSNA. Thus, we propose that NMDA receptors in PVN may facilitate ejaculation through enhancing the activity of sympathetic system.

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“…19,20 The paraventricular nucleus is an important component of the central neurocircuitry of the CSAR. 21,22 Our previous study has shown that RVLM superoxide anions are necessary for the CSAR, as well as for the enhanced effect of angiotensin (Ang) II on the CSAR in the paraventricular nucleus, suggesting an important role for the RVLM in CSAR control. 23 Ang-(1-7) is an important biologically active peptide in the renin-Ang system family and is involved in regulating sympathetic outflow and cardiovascular activity.…”

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Angiotensin-(1–7) in the Rostral Ventrolateral Medulla Modulates Enhanced Cardiac Sympathetic Afferent Reflex and Sympathetic Activation in Renovascular Hypertensive Rats

et al. 2013

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Abstract-Enhancement of the cardiac sympathetic afferent reflex (CSAR) contributes to sympathetic excitation in hypertension. The aim of the present study was to determine whether angiotensin (Ang)-(1-7) in the rostral ventrolateral medulla (RVLM) modulated the enhanced CSAR and sympathetic activation, and the signaling pathways that mediated these effects in the 2-kidney, 1-clip renovascular hypertension model. Cardiac sympathetic afferent reflex was evaluated using renal sympathetic nerve activity and mean arterial pressure responses to epicardial capsaicin application in anesthetized sinoaortic-denervated and cervical-vagotomized rats. RVLM microinjection of Ang-(1-7) induced greater increases in renal sympathetic nerve activity and mean arterial pressure, and greater enhancement in CSAR in 2-kidney, 1-clip rats than in sham-operated rats, which was blocked by Mas receptor antagonist A-779, adenylyl cyclase inhibitors SQ22536 and MDL-12,330A, and protein kinase A inhibitors rp-adenosine-3′,5′-cyclic monophosphorothionate and H-89. Mas receptor expression in RVLM was increased in 2-kidney, 1-clip rats. Treatment with A-779, SQ22536, MDL-12,330A, rp-adenosine-3′,5′-cyclic monophosphorothionate, or H-89 in RVLM inhibited CSAR and decreased renal sympathetic nerve activity and mean arterial pressure in 2-kidney, 1-clip rats, whereas cAMP analogue dibutyryl-cAMP had the opposite effects. Ang-(1-7) in RVLM increased, whereas A-779 decreased the cAMP level and the epicardial capsaicin application-induced increases in the cAMP level in RVLM. These results indicate that Ang-(1-7) in the RVLM enhances the CSAR and increases the sympathetic outflow and blood pressure via Mas receptor activation. The increased endogenous Ang-(1-7) and Mas receptor activity in RVLM contributes to the enhanced CSAR and sympathetic activation in renovascular hypertension, and the cAMP-protein kinase A pathway is involved in these Ang-(1-7)-mediated effects 24,30,31 Our recent study has shown that Ang-(1-7) in the RVLM enhances the CSAR and increases renal sympathetic nerve activity (RSNA) and mean arterial pressure (MAP), whereas A-779 microinjection into the RVLM decreases the RSNA and MAP and inhibits the CSAR in normal rats.32 However, it is not known whether Ang-(1-7) in the RVLM is involved in the enhanced CSAR and excessive sympathetic activation in hypertension.A recent study demonstrates that Mas receptor activation by Ang-(1-7) increases the intracellular cAMP level and activates protein kinase A (PKA) and that inhibition of either adenylyl cyclase (AC) or PKA activity attenuates Ang-(1-7)-induced extracellular signal-regulated kinase 1/2 activation in glomerular mesangial cells.33 Ang-(1-7) inhibits vascular growth via prostacyclin-mediated cAMP production and PKA activation. 34 These results demonstrate that the cAMP-PKA signaling pathway regulates Ang-(1-7) function in some peripheral tissues. However, whether the cAMP-PKA pathway is involved in Ang-(1-7)-mediated effects in the RVLM in hypertension is not well understood. The...

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Paraventricular nucleus is involved in the central pathway of cardiac sympathetic afferent reflex in rats

Cited by 65 publications

References 46 publications

Melanocortin receptor-mediated effects on obesity are distributed over specific hypothalamic regions

Melanocortin receptor-mediated effects on obesity are distributed over specific hypothalamic regions

Centrally mediated ejaculatory response via sympathetic outflow in rats: role of N‐methyl‐D‐aspartic acid receptors in paraventricular nucleus

Angiotensin-(1–7) in the Rostral Ventrolateral Medulla Modulates Enhanced Cardiac Sympathetic Afferent Reflex and Sympathetic Activation in Renovascular Hypertensive Rats

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