|Enhanced activation of RVLM-projecting PVN neurons in rats with chronic heart failure.|
|PMID: 22307669 Owner: NLM Status: MEDLINE|
|Previous studies have indicated that there is increased activation of the paraventricular nucleus (PVN) in rats with chronic heart failure (CHF); however, it is not clear if the preautonomic neurons within the PVN are specifically overactive. Also, it is not known if these neurons have altered responses to baroreceptor or osmotic challenges. Experiments were conducted in rats with CHF (6-8 wk after coronary artery ligation). Spontaneously active neurons were recorded in the PVN, of which 36% were antidromically activated from the rostral ventrolateral medulla (RVLM). The baseline discharge rate in RVLM-projecting PVN (PVN-RVLM) neurons from CHF rats was significantly greater than in sham-operated (sham) rats (6.0 ± 0.6 vs. 2.6 ± 0.3 spikes/s, P < 0.05). Picoinjection of the N-methyl-D-aspartate (NMDA) receptor antagonist D,L-2-amino-5-phosphonovaleric acid significantly decreased the basal discharge of PVN-RVLM neurons by 80% in CHF rats compared with 37% in sham rats. Fifty-two percent of spontaneously active PVN-RVLM neurons responded to changes in the mean arterial pressure (MAP). The changes in discharge rate in PVN-RVLM neurons after a reduction in MAP (+52 ± 7% vs. +184 ± 61%) or an increase in MAP (-42 ± 8% vs. -71 ± 6%) were significantly attenuated in rats with CHF compared with sham rats. Most PVN-RVLM neurons (63%), including all barosensitive PVN-RVLM neurons, were excited by an internal carotid artery injection of hypertonic NaCl (2.1 osmol/l), whereas a smaller number (7%) were inhibited. The increase in discharge rate in PVN-RVLM neurons to hypertonic stimulation was significantly enhanced in rats with CHF compared with sham rats (134 ± 15% vs. 92 ± 13%). Taken together, these data suggest that PVN-RVLM neurons are more active under basal conditions and this overactivation is mediated by an enhanced glutamatergic tone in rats with CHF. Furthermore, this enhanced activation of PVN-RVLM neurons may contribute to the altered responses to baroreceptor and osmotic challenges observed during CHF.|
|Bo Xu; Hong Zheng; Kaushik P Patel|
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|Type: Journal Article; Research Support, N.I.H., Extramural Date: 2012-02-03|
|Title: American journal of physiology. Heart and circulatory physiology Volume: 302 ISSN: 1522-1539 ISO Abbreviation: Am. J. Physiol. Heart Circ. Physiol. Publication Date: 2012 Apr|
|Created Date: 2012-04-16 Completed Date: 2012-05-30 Revised Date: 2013-06-26|
Medline Journal Info:
|Nlm Unique ID: 100901228 Medline TA: Am J Physiol Heart Circ Physiol Country: United States|
|Languages: eng Pagination: H1700-11 Citation Subset: IM|
|Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, Nebraska 68198-5850, USA.|
|APA/MLA Format Download EndNote Download BibTex|
Coronary Vessels / physiology
Enzyme Inhibitors / pharmacology
Excitatory Amino Acid Agonists / pharmacology
Excitatory Amino Acid Antagonists / pharmacology
Heart Failure / pathology*
Medulla Oblongata / cytology, physiology*
Midline Thalamic Nuclei / cytology, physiology*
N-Methylaspartate / pharmacology
Neurons / drug effects, physiology*
Nitric Oxide Synthase Type III / antagonists & inhibitors
Pressoreceptors / drug effects
omega-N-Methylarginine / pharmacology
|HL-62222/HL/NHLBI NIH HHS; P01 HL062222/HL/NHLBI NIH HHS|
|0/Enzyme Inhibitors; 0/Excitatory Amino Acid Agonists; 0/Excitatory Amino Acid Antagonists; 17035-90-4/omega-N-Methylarginine; 6384-92-5/N-Methylaspartate; 76726-92-6/2-Amino-5-phosphonovalerate; EC 18.104.22.168/Nitric Oxide Synthase Type III|
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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