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关于血管加压素诱导肾素释放抑制的机制。

On the mechanism of the vasopressin-induced inhibition of renin release.

作者信息

Knepel W, Reimann W, Nutto D

出版信息

Horm Metab Res. 1982 Mar;14(3):157-60. doi: 10.1055/s-2007-1018953.

Abstract

The isoprenaline-induced renin release was used to study both in vivo and in vitro and mechanism of the inhibitory effect of vasopressin on renin secretion. (1) The vasopressin analogue [1-deaminopenicillamine, 2-(0-methyl)-tyrosine]-arginine-vasopressin, which antagonizes the vasopressor response to vasopressin but possesses antidiuretic potency, abated the increase in plasma renin concentration following isoprenaline injection in the conscious rat without altering the fall in arterial blood pressure, (2) In a continuous superfusion system of rat kidney cortical slices, vasopressin in concentrations up to 10(-6) M failed to affect the isoprenaline-induced increase in renin secretion, which was evidently beta-adrenoceptor-mediated. In contrast, angiotensin II (10(-6) M) prevented the renin release in response to isoprenaline. These results led us to conclude that the inhibition of renin release caused by vasopressin is not necessarily related to its vasoconstrictor potency. The mechanism, through which vasopressin works, appears to differ from that of angiotensin II and is non functional in renal cortical slices.

摘要

采用异丙肾上腺素诱导的肾素释放来研究血管加压素对肾素分泌抑制作用的体内和体外机制。(1)血管加压素类似物[1-脱氨青霉胺,2-(O-甲基)-酪氨酸]-精氨酸血管加压素,可拮抗血管加压素的升压反应,但具有抗利尿作用,在清醒大鼠中,该类似物可减轻异丙肾上腺素注射后血浆肾素浓度的升高,而不改变动脉血压的下降;(2)在大鼠肾皮质切片连续灌流系统中,浓度高达10(-6)M的血管加压素未能影响异丙肾上腺素诱导的肾素分泌增加,后者显然是由β-肾上腺素能受体介导的。相比之下,血管紧张素II(10(-6)M)可抑制异丙肾上腺素诱导的肾素释放。这些结果使我们得出结论,血管加压素引起的肾素释放抑制不一定与其血管收缩作用相关。血管加压素发挥作用的机制似乎不同于血管紧张素II,且在肾皮质切片中不起作用。

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