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肾素缺乏导致肾血流与滤过率自身调节的分离。

Dissociation of renal blood flow and filtration rate autoregulation by renin depletion.

作者信息

Hall J E, Guyton A C, Cowley A W

出版信息

Am J Physiol. 1977 Mar;232(3):F215-21. doi: 10.1152/ajprenal.1977.232.3.F215.

DOI:10.1152/ajprenal.1977.232.3.F215
PMID:842668
Abstract

Renal blood flow (RBF) and glomerular filtration rate (GFR) autoregulation during changes in renal artery pressure (RAP) were examined in dogs fed a "normal" diet (group 1, n = 10) and in renin-depleted dogs (group 2, n = 11) which received a high-sodium diet and deoxycorticosterone acetate (DOCA) injections for a minimum of 21 days prior to the study. Renal venous plasma renin activity was undetectable in group 2 by radioimmunoassay of angiotensin I and did not increase even when RAP was reduced to less than 70 mmHg. Autoregulation of RBF was not impaired by renin depletion. However, GFR autoregulation, which was very effective in group 1 dogs, was markedly impaired in group 2. Average GFR in group 2 decreased progressively to 58 +/- 7% of the control value as RAP was reduced in steps from the control value of 137 +/- 3 to 69 +/- 1 mmHg. In normal dogs, the filtration fraction either increased slightly or did not change when RAP was reduced in steps, whereas in renin-depleted dogs the filtration fraction decreased progressively during reductions in RAP. Thus, chronic sodium loading and DOCA administration causes renin depletion and dissociates the autoregulation of RBF and GFR. These data are consistent with the hypothesis that the renin-angiotensin system participates in the control of GFR, possibly by an efferent arteriolar mechanism.

摘要

在喂食“正常”饮食的犬类(第1组,n = 10)以及肾素耗竭的犬类(第2组,n = 11)中,研究了肾动脉压(RAP)变化期间的肾血流量(RBF)和肾小球滤过率(GFR)自身调节。第2组犬类在研究前至少21天接受高钠饮食和醋酸脱氧皮质酮(DOCA)注射,通过放射免疫分析法检测血管紧张素I,发现第2组肾静脉血浆肾素活性无法检测到,即使RAP降至低于70 mmHg时也未增加。肾素耗竭并未损害RBF的自身调节。然而,第1组犬类中非常有效的GFR自身调节在第2组中明显受损。随着RAP从137±3 mmHg的对照值逐步降至69±1 mmHg,第2组的平均GFR逐渐降至对照值的58±7%。在正常犬类中,当RAP逐步降低时,滤过分数略有增加或不变,而在肾素耗竭的犬类中,随着RAP降低,滤过分数逐渐下降。因此,长期钠负荷和DOCA给药会导致肾素耗竭,并使RBF和GFR的自身调节分离。这些数据与肾素 - 血管紧张素系统可能通过出球小动脉机制参与GFR控制的假设一致。

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