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在大鼠中,反复颅内注射血管紧张素 II(AngII)会损害其饮水和肾脏的反应。

Impaired dipsogenic and renal response to repetitive intracerebroventricular angiotensin II (AngII) injections in rats.

机构信息

Disciplina de Medicina Interna, Laboratório de Metabolismo Hidro-Salino, Núcleo de Medicina e Cirurgia Experimental, Departamento de Clínica Médica, Faculdade de Ciências Médicas, Universidade Estadual de Campinas, Sao Paolo, Brazil.

出版信息

J Renin Angiotensin Aldosterone Syst. 2011 Sep;12(3):161-8. doi: 10.1177/1470320310392617. Epub 2011 Mar 10.

Abstract

The role of the central nervous system (CNS) in the control of blood pressure and hydrosaline homeostasis has been demonstrated by several studies. While circulating angiotensin II (AngII) tends to retain sodium by a direct renal action as well as through aldosterone release, stimulation of brain AngII receptors has been reported to induce natriuresis. Repetitive intracerebroventricular AngII injection was recently demonstrated to be capable of leading to desensitisation of the dipsogenic effect of AngII stimuli. The aim of the current study was to investigate a possible central desensitisation to AngII stimuli by observing the effects of a low-concentration solution of AngII on the dipsogenic and natriuretic mechanisms in conscious rats, compared with appropriate age-matched 0.15 M NaCl-injected subjects, as evaluated by lithium clearance. The present report confirmed earlier reports on the potent natriuretic and dipsogenic effects of central AngII receptor stimulation. Natriuresis is mediated by a decrease in sodium reabsorption in the proximal and post-proximal tubule segments of the nephron. The current findings lend further support to the idea that AngII, in the CNS, is instrumental in the regulation of body fluid homeostasis. The magnitude of the dipsogenic and renal response to AngII was significantly decreased by repetitive stimulus.

摘要

已有多项研究证明了中枢神经系统(CNS)在血压和水盐稳态控制中的作用。虽然循环血管紧张素 II(AngII)通过直接的肾脏作用以及醛固酮释放来保留钠,但据报道,大脑 AngII 受体的刺激会引起利钠作用。最近的研究表明,重复脑室内注射 AngII 能够导致 AngII 刺激的渴觉作用脱敏。本研究的目的是通过观察低浓度 AngII 溶液对清醒大鼠的渴觉和利钠机制的影响,来研究中枢对 AngII 刺激的可能脱敏作用,与适当的年龄匹配的 0.15 M NaCl 注射组进行比较,通过锂清除率进行评估。本报告证实了先前关于中枢 AngII 受体刺激具有强大的利钠和渴觉作用的报告。利钠作用是通过减少肾单位近端和近段小管段的钠重吸收来介导的。目前的研究结果进一步支持了这样一种观点,即在中枢神经系统中,AngII 在调节体液稳态中起着重要作用。对 AngII 的渴觉和肾脏反应的幅度通过重复刺激显著降低。

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