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血管加压素对肾激肽释放酶排泄的影响。

Effect of vasopressin on renal kallikrein excretion.

作者信息

Fejes-Tóth G, Zahajszky T, Filep J

出版信息

Am J Physiol. 1980 Oct;239(4):F388-F392. doi: 10.1152/ajprenal.1980.239.4.F388.

Abstract

In an attempt to investigate a possible interaction between vasopressin and the renal kallikrein-kinin system, renal function and urinary kallikrein excretion were monitored in trained conscious dogs and in anesthetized rats in water diuresis and in vasopressin-induced antidiuresis. Vasopressin elevated urinary kallikrein excretion in a dose-dependent way in both species, with concomitant increases in urinary osmolality and electrolyte excretion. A significant increase in kallikrein excretion was observed with a dose of vasopressin as low as 2 mU . kg-1 . h-1 in the dog and 3 mU . kg-1 . h-1 in the rat without a change in renal hemodynamics. In the rat vasopressin-induced changes in kallikrein excretion were positively correlated with changes in sodium and potassium excretion and negatively correlated with changes in free water clearance. It is concluded that vasopressin over its normal physiological range of concentration stimulates renal kallikrein secretion.

摘要

为了研究血管加压素与肾脏激肽释放酶-激肽系统之间可能存在的相互作用,在训练有素的清醒犬以及麻醉大鼠处于水利尿和血管加压素诱导的抗利尿状态下,对其肾功能和尿激肽释放酶排泄情况进行了监测。在这两种动物中,血管加压素均以剂量依赖的方式提高尿激肽释放酶排泄量,同时尿渗透压和电解质排泄也随之增加。在犬中,当血管加压素剂量低至2 mU·kg-1·h-1 ,在大鼠中低至3 mU·kg-1·h-1时,即可观察到激肽释放酶排泄量显著增加,而肾血流动力学并无变化。在大鼠中,血管加压素诱导的激肽释放酶排泄变化与钠和钾排泄变化呈正相关,与自由水清除率变化呈负相关。得出的结论是,血管加压素在其正常生理浓度范围内可刺激肾脏激肽释放酶分泌。

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