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[计划性血液透析终末期肾衰竭患者的高血压发病机制]

[Mechanisms of hypertension in patients with terminal kidney failure on programmed hemodialysis].

作者信息

Krimkevich E I, Petrun' N M, Baran E Ia, Kutsaĭ N N, Khomenko N V

出版信息

Ter Arkh. 1986;58(8):81-4.

PMID:3020729
Abstract

The state of some mechanisms involved in AP regulation was studied in 18 patients with terminal renal failure (TRF) on programmed hemodialysis for 7-9 mos. The imbalance of extra- and intracellular sodium, potassium and water causing hypertension, was noted in TRF patients. TRF patients revealed (against a background of the normal activity of plasma renin) a high activity of carboxycathepsin resulting in the creation of conditions for enhanced kinin degradation playing a depressor role and for intense angiotensin II formation, being an important mechanism of persistent hypertension. An increase in the activity of carboxycathepsin can be one of the reasons of hyperaldosteronemia detected in the patients. A single session of hemodialysis does not significantly influence the activity of carboxycathepsin.

摘要

对18例接受7 - 9个月程序性血液透析的终末期肾衰竭(TRF)患者体内一些参与血压调节的机制状态进行了研究。TRF患者存在细胞内外钠、钾和水的失衡,这会导致高血压。TRF患者(在血浆肾素活性正常的背景下)显示羧基组织蛋白酶活性较高,这导致了有利于增强激肽降解(发挥降压作用)以及强烈的血管紧张素II形成的条件,而血管紧张素II形成是持续性高血压的重要机制。羧基组织蛋白酶活性增加可能是患者中检测到的醛固酮增多症的原因之一。单次血液透析对羧基组织蛋白酶的活性没有显著影响。

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