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氯沙坦可阻断大鼠体内由中枢鸟氨酸血管加压素诱导的饮水行为和cFos表达。

Losartan blocks drinking and cFos expression induced by central ornithine vasotocin in rats.

作者信息

Fitts Douglas A, Zierath Dannielle K, Wilkins Emily E, Bassett John E

机构信息

Department of Psychology, University of Washington, Box 351525, Seattle, WA 98195-1525, USA.

出版信息

Physiol Behav. 2005 Nov 15;86(4):573-7. doi: 10.1016/j.physbeh.2005.08.027. Epub 2005 Oct 5.

Abstract

We previously reported that an intracerebroventricular (icv) injection of the oxytocin receptor antagonist ornithine vasotocin (OVT) caused water and saline intakes, a pressor response, and Fos-like immunoreactivity (Fos-IR) in the median preoptic nucleus of the rat brain. In the present report, rats receiving an icv injection of isotonic saline vehicle followed by an icv injection of 10 microg of OVT 20 min later drank 5.5+/-1.1 ml of total water and saline intake in 60 min after the OVT; rats receiving 10 microg of losartan before the OVT drank only 0.9+/-0.3 ml of total fluid. In a separate study, rats were treated as above except that they were not allowed to drink and were perfused for analysis of Fos-IR in the median preoptic nucleus at 90 min. Fos-IR in the dorsal part of the median preoptic nucleus was significantly suppressed from 2.69+/-0.57 cells per 10,000 square mum in vehicle-treated rats to 0.89+/-0.20 in losartan-treated rats. Losartan alone had no effect on Fos-IR. Losartan did not reduce intake of saccharin in a dessert test. This suggests that the OVT-induced drinking may result from an activation or disinhibition of angiotensin type AT1 receptors in the median preoptic nucleus.

摘要

我们之前报道过,脑室内(icv)注射催产素受体拮抗剂鸟氨酸加压素(OVT)会导致大鼠饮水和摄入生理盐水、出现升压反应,并在大鼠脑的视前正中核产生Fos样免疫反应(Fos-IR)。在本报告中,先接受icv注射等渗盐水载体,20分钟后再接受icv注射10微克OVT的大鼠,在注射OVT后的60分钟内总饮水量和生理盐水摄入量为5.5±1.1毫升;在注射OVT前接受10微克氯沙坦的大鼠,总液体摄入量仅为0.9±0.3毫升。在另一项研究中,大鼠的处理方式与上述相同,只是不允许它们饮水,并在90分钟时进行灌注,以分析视前正中核中的Fos-IR。视前正中核背侧部分的Fos-IR从接受载体处理的大鼠每10000平方微米2.69±0.57个细胞显著抑制至接受氯沙坦处理的大鼠的0.89±0.20个细胞。单独使用氯沙坦对Fos-IR没有影响。在甜品测试中,氯沙坦不降低糖精的摄入量。这表明OVT诱导的饮水可能是由于视前正中核中血管紧张素AT1受体的激活或去抑制所致。

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