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加压剂量的血管紧张素II对大鼠肾小球滤过率的自身调节及肾内分布的影响。

The effect of pressor doses of Angiotensin II on autoregulation and intrarenal distribution of glomerular filtration rate in the rat.

作者信息

Göransson A, Sjöquist M

出版信息

Acta Physiol Scand. 1984 Dec;122(4):615-20. doi: 10.1111/j.1748-1716.1984.tb07551.x.

Abstract

This study was designed to investigate the effect of pressor doses of exogenous Angiotensin II (AII) on autoregulation and intrarenal distribution of single nephron glomerular filtration rate (SNGFR) in anesthetized, normotensive rats. SNGFR at all cortical levels of the left kidney was measured with a modified Hanssen technique at three renal arterial pressures (RAP): Spontaneous, 100 +/- 1 mmHg and 70 +/- 1 mmHg. In control rats, both outer cortical (OC) and inner cortical (IC) nephrons showed complete autoregulation of SNGFR when RAP was reduced to 100 +/- 1 mmHg. Further reduction to 70 +/- 1 mmHg resulted in different responses among the cortical layers, accompanying a decrease in SNGFR. The SNGFRIC/SNGFROC ratio increased from 1.36 +/- 0.053 to 1.52 +/- 0.047 and a fractional redistribution of glomerular filtration rate towards IC nephrons was seen. When the kidney was submitted to a RAP of 70 +/- 1 mmHg, there was a concomitant increase in central arterial pressure (CAP) from 120 +/- 4.3 to 134 +/- 3.2 mmHg. A continuous i.v. infusion of AII (0.5 microgram . min-1 . kg-1 BW) increased mean arterial pressure from 123 +/- 1.4 to 142 +/- 3.8 mmHg, an effect corresponding to that on peripheral vascular resistance during reduction of RAP to 70 +/- 1 mmHg in control rats. This dose reduced SNGFR at all cortical levels, but did not per se lead to redistribution of SNGFR. A reduction in RAP to 100 +/- 1 mmHg during AII administration resulted in impaired autoregulation of SNGFR in both OC and IC nephrons.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

本研究旨在探讨麻醉状态下的正常血压大鼠中,外源性血管紧张素II(AII)的升压剂量对单肾单位肾小球滤过率(SNGFR)的自身调节及肾内分布的影响。采用改良的汉森技术,在三个肾动脉压(RAP)水平下测量左肾所有皮质层面的SNGFR:自主血压、100±1 mmHg和70±1 mmHg。在对照大鼠中,当RAP降至100±1 mmHg时,外皮质(OC)和内皮质(IC)肾单位的SNGFR均表现出完全的自身调节。进一步降至70±1 mmHg时,各皮质层出现不同反应,同时SNGFR降低。SNGFRIC/SNGFROC比值从1.36±0.053增加至1.52±0.047,肾小球滤过率出现向IC肾单位的部分重新分布。当肾脏处于70±1 mmHg的RAP时,中心动脉压(CAP)从120±4.3 mmHg伴随性升高至134±3.2 mmHg。持续静脉输注AII(0.5微克·分钟-1·千克-1体重)使平均动脉压从123±1.4 mmHg升高至142±3.8 mmHg,这一效应与对照大鼠中RAP降至70±1 mmHg时对外周血管阻力的影响相当。该剂量降低了所有皮质层面的SNGFR,但本身并未导致SNGFR的重新分布。在输注AII期间将RAP降至100±1 mmHg会导致OC和IC肾单位的SNGFR自身调节受损。(摘要截选至250字)

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