低肾素性原发性高血压的机制探讨  

APPROACH TO THE MECHANISM OF "LOW-RENIN" ESSENTIAL HYPERTENSION

作　　者：赵光胜[1] 李迪元[1] 孔德汶[1] 王政[1] 陈贤妙 黄友文[1] 曹素玲[1] 庞庆祥[1] 

机构地区：[1]上海第二医科大学

出　　处：《上海医学》1989年第7期392-294,共1页Shanghai Medical Journal

摘　　要：低肾素性原发性高血压可能属于特定的临床和病理生理类型。本文比较低PRA与非低PRA性EH组在快速静滴盐水1000ml前后血浆血压调控激素、红细胞膜阳离子转运功能和膜结构变化。发现低PRA性者:(1)在盐水前的PA明显较高:PRA/PA较低。(2)负荷盐水期的尿排Na和K较少、盐水后红细胞膜向外Na^+-K^+协同转运较低,均趋潴Na。(3)盐水后PA仍较高,PRA及PRA/PA均较低。认为低PRA性EH的特点之一是细胞内外潴Na;值得对其肾素-血管紧张素-醛固酮-ACTH-多巴胺能系统间关系失调机制作进一步探索。'Low Renin' essential hypertension seems to be an unique clinical and pathophysiological category. Thirteen cases (21%) were found to be this sub-type taking plasma renin activity PRA<0.2 ng/ml/h as standard in 48 male essential hypertensives (40—59 years of age). The hormones modulating blood-pressure, erythrocyte membrane cation transport functions and configuration patterns before and after rapid 1000 ml intravenous salineloading were compared between 'Low-Renin' and non-'Low-Renin' groups. Results showed: (1) plasma aldosterone (PA) level was significantly higher, while PRA/PA was lower in 'Low-Renin' group before saline-loading; (2) urinary sodium and potassium output was less during saline-loading, the erythrocyte outward sodium and potassum cotransport and PRA (PRB/PA) were lower after saline-loading tending to sodiumretention. One of the characteristics of 'Low-Renin' group might be susceptible to sodium-retention inside and outside of the cell, and the mechanism among renin-anigiotension-aldosterone-ACTH-dopamine systems should be further explored.

关 键 词：低肾素 原发性高血压 机制 

分 类 号：R544.150.2[医药卫生—心血管疾病]