3.8 Article

Modulation of the carotid baroreceptor reflex by substance P in the nucleus tractus solitarius

期刊

JOURNAL OF THE AUTONOMIC NERVOUS SYSTEM
卷 78, 期 2-3, 页码 77-85

出版社

ELSEVIER SCIENCE BV
DOI: 10.1016/S0165-1838(99)00060-0

关键词

baroreflex; baroreceptors; substance P; neuropeptides; NTS

资金

  1. NHLBI NIH HHS [HL55490] Funding Source: Medline

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Previous studies have shown that administration of substance P (SP) into the nucleus tractus solitarius (NTS) can evoke a depressor response similar to that produced by activation of the arterial baroreceptors. In addition, some studies have suggested that SP increases the reflex responses to activation of baroreceptor input. The present study was performed to determine the effects of SP on the carotid sinus baroreceptor reflex at the level of the NTS by examining the effects of both exogenous SP microinjected into different rostrocaudal locations in the NTS and blockade of the effects of endogenous SP, through the microinjection of a substance P antagonist (SPa; [D-Pro, D-Trp]-substance P). Changes in pressure in an isolated carotid sinus in anesthetized dogs were used to evoke baroreflex changes in arterial blood pressure (BP) before and after microinjection of SP (0.5 mu M) or SPa (10 mu M) into barosensitive regions of the NTS. Microinjection of SP or its antagonist did not alter baseline, resting BP but did produce significant changes in baroreflex sensitivity. Microinjection of SP into different rostrocaudal regions of the NTS produced different responses, with rostral and caudal NTS microinjections producing significant increases in sensitivity. No effects on baroreflex sensitivity were obtained in response to SP microinjections into the intermediate NTS. Unlike SP, microinjection of the SPa significantly decreased baroreflex sensitivity at all rostrocaudal levels of the NTS. These data demonstrated that SP has the capability to modulate the carotid baroreflex at the level of the NTS and support a physiological role for endogenously released SP. (C) 2000 Published by Elsevier Science B.V. All rights reserved.

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