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肾动脉狭窄后对侧多尿机制的研究。

Studies of the mechanism of contralateral polyuria after renal artery stenosis.

作者信息

Galvez O G, Roberts B W, Mishkind M H, Bay W H, Ferris T F

出版信息

J Clin Invest. 1977 Apr;59(4):609-15. doi: 10.1172/JCI108678.

Abstract

Acute renal artery stenosis in hydropenic dogs caused a contralateral increase in urine volume and free water clearance without change in glomerular filtration, renal blood flow, or osmolar clearance. The increase in urine volume was not dependent on the development of hypertension since it occurred in animals pretreated with trimethaphan but was dependent upon angiotensin since it was presented with angiotensin blockade with Saralasin. The effect was not caused by angiotensin inhibiting antidiuretic hormone release since the polyuria occurred in hypophysectomized animals receiving a constant infusion of 10 muU/kg per min of aqueous Pitressin. Since the rise in urine volume was associated with an increase in renal vein prostaglandin E concentration and was prevented by pretreatment with indomethacin (5 mg/kg) the results suggest that the rise in plasma angiotensin after renal artery stenosis causes an increase in contralateral prostaglandin E synthesis with resultant antagonism to antidiuretic hormone at the collecting tubule.

摘要

缺水犬的急性肾动脉狭窄导致对侧尿量增加和自由水清除率增加,而肾小球滤过、肾血流量或渗透清除率无变化。尿量增加不依赖于高血压的发展,因为它发生在用三甲噻芬预处理的动物中,但依赖于血管紧张素,因为它在使用沙拉新进行血管紧张素阻断时出现。这种效应不是由血管紧张素抑制抗利尿激素释放引起的,因为多尿发生在接受每分钟10微单位/千克垂体后叶素持续输注的垂体切除动物中。由于尿量增加与肾静脉前列腺素E浓度增加有关,并且通过吲哚美辛(5毫克/千克)预处理可预防,结果表明肾动脉狭窄后血浆血管紧张素升高导致对侧前列腺素E合成增加,从而在集合管对抗抗利尿激素。

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