格列本脲敏感的钾通道负责低钠大鼠肾小球中血管紧张素II超敏收缩和心房利钠因子不应性。

Glibenclamid-sensitive K+ channels are responsible for angiotensin II hypersensitive contraction and atrial natriuretic factor refractoriness of glomeruli in low-sodium rats.

作者信息

Szczepańska-Konkel M, Redlak M, Angielski S

机构信息

Department of Clinical Biochemistry, Medical Academy, Gdańsk, Poland.

出版信息

Biochem Biophys Res Commun. 1991 Dec 16;181(2):871-6. doi: 10.1016/0006-291x(91)91271-d.

DOI:10.1016/0006-291x(91)91271-d

PMID:1836728

Abstract

We investigated the role of ANF and potassium channels in dynamics of glomeruli isolated from low and normal-sodium rats. The ANG II-induced decrease glomerular size (36%) and (18%) in low and normal-sodium rats, respectively. ANF or cicletanine showed reversing effect on the ANG II-precontracted glomeruli from normal but not from low-sodium rats. The action of ANG II was abolished when ANF and cicletanine were added together. Glibenclamid completely abolished the inhibitory effect of cicletanine and ANF on ANG II-induced contraction of glomeruli from low-sodium rats. These results suggest that glibenclamid-sensitive potassium channels are responsible for ANG II hypersensitive contraction and ANF or cicletanine refractoriness of isolated glomeruli from low-sodium rats.

摘要

我们研究了心房钠尿肽（ANF）和钾通道在低钠和正常钠大鼠分离肾小球动力学中的作用。血管紧张素II（ANG II）分别使低钠和正常钠大鼠的肾小球大小减小36%和18%。ANF或西氯他宁对正常钠大鼠而非低钠大鼠的ANG II预收缩肾小球有逆转作用。当将ANF和西氯他宁一起添加时，ANG II的作用被消除。格列本脲完全消除了西氯他宁和ANF对低钠大鼠ANG II诱导的肾小球收缩的抑制作用。这些结果表明，格列本脲敏感的钾通道负责低钠大鼠分离肾小球的ANG II超敏收缩以及ANF或西氯他宁难治性。