卡托普利抑制血管紧张素II前后PGE2输注对正常人肾功能的影响。

Renal physiology Pub Date : 1987-01-01 DOI:10.1159/000173137
M Usberti, B Cianciaruso, G Di Minno, A Auciello, G Ardillo, D Bonanno, G Conte, V E Andreucci
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引用次数: 2

摘要

7名正常志愿者在卡托普利抑制血管紧张素II合成(100mg)前后,分别递增剂量(5、10、20、40、60 ng/kg/min)输注前列腺素E2 (PGE2)。单独输注PGE2不改变血压,但增加尿中肾上腺素和去甲肾上腺素的排泄,增强对氨基低尿酸清除率(CPAH)、菊粉清除率(CIn)、钠和水的排泄,降低尿渗透压。卡托普利单独用药后,CIn、CPAH和儿茶酚胺未见变化,但尿量和钠排泄量明显增加,尿渗透压下降。在卡托普利存在的情况下,输注PGE2导致血压和CIn明显下降,肾上腺素和钠排泄增加,而CPAH没有明显降低。我们的研究结果表明,完整的肾素-血管紧张素系统对于维持PGE2输注期间的GFR是必要的。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Effects of PGE2 infusion on renal function in normal man before and after angiotensin II inhibition by captopril.

Increasing doses of prostaglandin E2 (PGE2) (5, 10, 20, 40, 60 ng/kg/min) were infused in 7 normal volunteers before and after angiotensin II synthesis inhibition by captopril (100 mg by mouth). PGE2 infusion alone did not alter blood pressure, while it increased the urinary excretion of both epinephrine and norepinephrine, enhanced p-aminohyppuric clearance (CPAH), inulin clearance (CIn), sodium and water excretion and decreased urinary osmolality. No changes of CIn, CPAH and catecholamines were observed after captopril alone, whilst there was a significant increase in urine output and sodium excretion and a decrease in urinary osmolality. In the presence of captopril, the infusion of PGE2 caused a significant fall in blood pressure and CIn, enhanced epinephrine excretion and sodium excretion, while it did not significantly reduce CPAH. Our findings suggest that an intact renin-angiotensin system is necessary to maintain GFR during PGE2 infusion.

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