论文部分内容阅读
巴特氏综合征主要表现为低血钾性碱中毒,肾素及醛固酮分泌增多,肾小球旁体细胞(JG)增生。尽管是高肾素、高醛固酮血症,但具有血压正常,静注血管紧张素Ⅱ(AⅡ)也无升压反应等特征。最初Bartter 等认为其病因主要是血管对AⅡ不敏感所致,但以后发现了很多病例血管敏感性低下是可逆的。本症是否与激素受体的异常有关呢?还有很多问题目前尚不十分清楚。本文就有关病因方面作一概述。一、巴特氏综合征病因学说的进展Bartter 过去认为AⅡ不能使血管升压反应亢进,血压不升高是先天性缺陷。一般认为
Butte’s syndrome is mainly hypokalemic alkalosis, increased secretion of renin and aldosterone, and proliferation of glomerular paracrine somatic cells (JG). Despite its high renin and hyperaldosteronism, it has the characteristics of normal blood pressure and intravenous infusion of angiotensin Ⅱ (AⅡ). Bartter et al. First thought that the etiology was mainly caused by the fact that blood vessels were not sensitive to AII, but later found that many cases of vascular sensitivity is reversible. Is the disorder related to the abnormality of the hormone receptor? There are many problems that are not yet clear. This article gives an overview of the etiology. First, the progress of the etiology of Bartter syndrome Bartter in the past that A Ⅱ can not make the blood pressure response hyperactivity, blood pressure is not elevated congenital defects. Generally considered