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卡托普利抑制转化酶期间肾小球血流的自身调节。

Autoregulation of glomerular blood flow during converting-enzyme inhibition by captopril.

作者信息

Steinhausen M, Holz F G

机构信息

I. Physiologisches Institut, Universität Heidelberg, Federal Republic of Germany.

出版信息

Biomed Biochim Acta. 1987;46(12):1005-9.

PMID:3330936
Abstract

We investigated the effects of local angiotensin-converting enzyme (ACE) inhibition by captopril on the autoregulatory efficiency of glomerular blood flow (GBF). The microvasculature of the nonfiltering rat kidney was observed via in vivo television microscopy. Clamping of the aorta above the renal arteries allowed controlled reductions in renal perfusion pressure. Perfusion pressure reductions (PPR) dilated preglomerular vessels and, within the autoregulatory range, GBF was well maintained. Local captopril application markedly attenuated pressure dependent vasodilation and abolished autoregulation of GBF. Autoregulatory response could be restored in the presence of captopril by adding angiotensin II (A II) to the tissue bath. These results indicate that autoregulation of GBF in the rat kidney is, at least partially, dependent on intrarenal renin-angiotensin activity.

摘要

我们研究了卡托普利对局部血管紧张素转换酶(ACE)的抑制作用对肾小球血流(GBF)自身调节效率的影响。通过体内电视显微镜观察未滤过大鼠肾脏的微血管。夹住肾动脉上方的主动脉可控制降低肾灌注压。灌注压降低(PPR)使肾小球前血管扩张,并且在自身调节范围内,GBF得到良好维持。局部应用卡托普利可显著减弱压力依赖性血管舒张,并消除GBF的自身调节。在组织浴中添加血管紧张素II(A II)可在存在卡托普利的情况下恢复自身调节反应。这些结果表明,大鼠肾脏中GBF的自身调节至少部分依赖于肾内肾素-血管紧张素活性。

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