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依那普利对慢性单肾高血压的肾脏及全身影响

Renal and systemic effects of enalapril in chronic one-kidney hypertension.

作者信息

Woods R L, Anderson W P, Korner P I

出版信息

Hypertension. 1986 Feb;8(2):109-16. doi: 10.1161/01.hyp.8.2.109.

Abstract

We have investigated the role of angiotensin II in the development of high blood pressure and in the maintenance of renal function during 2 weeks of one-kidney renal artery stenosis in conscious dogs. Responses to a fixed degree of inflation of a balloon cuff around the renal artery were compared in dogs with or without continuous enalapril (MK 421) treatment. In six untreated dogs, mean aortic pressure was increased by 17.1 +/- 2.0 mm Hg, due primarily to increases in total peripheral resistance with little change in cardiac output, while glomerular filtration rate, renal blood flow, renal artery pressure, and plasma renin activity were back to prestenosis levels. In seven enalapril-treated dogs mean aortic pressure was increased by 23.0 +/- 2.7 mm Hg and was not significantly different from that occurring in untreated dogs. This rise was due to increases in total peripheral resistance (10%) and cardiac output (12%). In the absence of angiotensin II, glomerular filtration rate remained low, at only 56 +/- 6% of prestenosis levels. Renal blood flow returned to normal, but the renal artery pressure remained 25% lower than control values. Thus, the main role of angiotensin II in chronic one-kidney Goldblatt hypertension does not appear to be through its pressor properties but rather through its actions in the kidney to preserve glomerular filtration. This effect on renal function persisted throughout the course of the hypertension, even when the plasma renin levels returned to normal.

摘要

我们研究了血管紧张素II在清醒犬一侧肾动脉狭窄2周期间高血压发展及肾功能维持中的作用。比较了接受或未接受依那普利(MK 421)持续治疗的犬对围绕肾动脉的气囊袖带固定程度充气的反应。在6只未治疗的犬中,平均主动脉压升高了17.1±2.0 mmHg,主要是由于总外周阻力增加,心输出量变化不大,而肾小球滤过率、肾血流量、肾动脉压和血浆肾素活性恢复到狭窄前水平。在7只接受依那普利治疗的犬中,平均主动脉压升高了23.0±2.7 mmHg,与未治疗犬的升高值无显著差异。这种升高是由于总外周阻力增加(10%)和心输出量增加(12%)。在缺乏血管紧张素II的情况下,肾小球滤过率仍然很低,仅为狭窄前水平的56±6%。肾血流量恢复正常,但肾动脉压仍比对照值低25%。因此,血管紧张素II在慢性一侧肾性Goldblatt高血压中的主要作用似乎不是通过其升压特性,而是通过其在肾脏中保留肾小球滤过的作用。即使血浆肾素水平恢复正常,这种对肾功能的影响在高血压病程中持续存在。

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