血管紧张素II抑制不足会调节人体左心室结构。

Inadequate suppression of angiotensin II modulates left ventricular structure in humans.

作者信息

Schlaich M P, Schobel H P, Langenfeld M R, Hilgers K, Schmieder R E

机构信息

Department of Medicine IV/Nephrology, University of Erlangen-Nürnberg, Germany.

出版信息

Clin Nephrol. 1998 Mar;49(3):153-9.

PMID:9543596

Abstract

BACKGROUND

In a previous study we found that high angiotensin II levels in relation to the corresponding urinary sodium excretion aggravate left ventricular hypertrophy in hypertensive patients. To analyze whether a dysregulation of the renin angiotensin aldosterone system determines left ventricular structure in young individuals, we examined whether the response of angiotensin II after increasing salt intake is related to left ventricular structure.

METHODS

In 51 young, male Caucasians with normal or mildly elevated blood pressure, left ventricular structure, 24-hour ambulatory blood pressure and dietary sodium intake (as estimated by 24-hour sodium excretion) were determined in parallel with plasma renin activity, angiotensin II, and aldosterone concentrations. Angiotensin II concentration and 24-hour sodium excretion were measured twice: firstly on a normal Bavarian diet and secondly at high salt intake to determine the resulting suppression of the renin-angiotensin-aldosterone system.

RESULTS

Body mass index (r = 0.42, p < 0.001) and both systolic (r = 0.28, p < 0.05) and diastolic (r = 0.25, p < 0.05) 24-hour ambulatory blood pressure correlated with left ventricular mass. No direct relationship was found between left ventricular structure and baseline angiotensin II concentration. The lower the physiological decrease of angiotensin II after high oral salt intake, i.e. the higher the angiotensin II level after salt intake remained, the greater was left ventricular mass (r = 0.38; p < 0.006) even after taking 24-hour ambulatory blood pressure into account (partial correlation; r = 0.43, p < 0.005). Consistently, angiotensin II concentration at high salt intake correlated with left ventricular mass independently of ambulatory blood pressure (partial correlation: r = 0.29, p < 0.05). Subgroup analysis revealed that the increase in sodium excretion at high salt intake was related to the decrease in angiotensin II levels in normotensive (r = -0.43, p < 0.05), but not in hypertensive subjects (r = 0.16, n.s.). The changes in angiotensin II concentration at high salt intake were related to left ventricular mass in hypertensive (r = 0.43, p < 0.02), but not in normotensive individuals (r = 0.21, n.s.).

CONCLUSION

Our finding that angiotensin II concentration at high salt intake correlated with left ventricular mass independently of ambulatory blood pressure suggests that inadequate suppression of angiotensin II after high salt intake contributes to left ventricular hypertrophy already in young hypertensive individuals independently of blood pressure.

摘要

背景

在之前的一项研究中，我们发现与相应尿钠排泄相关的高血管紧张素II水平会加重高血压患者的左心室肥厚。为了分析肾素 - 血管紧张素 - 醛固酮系统的失调是否决定年轻人的左心室结构，我们研究了增加盐摄入后血管紧张素II的反应是否与左心室结构相关。

方法

在51名血压正常或轻度升高的年轻男性白种人中，同时测定左心室结构、24小时动态血压和饮食钠摄入量（通过24小时尿钠排泄估算）以及血浆肾素活性、血管紧张素II和醛固酮浓度。血管紧张素II浓度和24小时尿钠排泄测定两次：首先在正常的巴伐利亚饮食下，其次在高盐摄入时，以确定肾素 - 血管紧张素 - 醛固酮系统由此产生的抑制作用。

结果

体重指数（r = 0.42，p < 0.001）以及收缩压（r = 0.28，p < 0.05）和舒张压（r = 0.25，p < 0.05）的24小时动态血压与左心室质量相关。未发现左心室结构与基线血管紧张素II浓度之间存在直接关系。高盐摄入后血管紧张素II的生理性下降越低，即盐摄入后血管紧张素II水平保持越高，左心室质量越大（r = 0.38；p < 0.006），即使考虑24小时动态血压后也是如此（偏相关；r = 0.43，p < 0.005）。同样，高盐摄入时的血管紧张素II浓度与左心室质量相关，独立于动态血压（偏相关：r = 0.29，p < 0.05）。亚组分析显示，高盐摄入时尿钠排泄的增加与血压正常者（r = -0.43，p < 0.05）血管紧张素II水平的降低相关，但与高血压患者无关（r = 0.16，无统计学意义）。高盐摄入时血管紧张素II浓度的变化与高血压患者（r = 0.43，p < 0.02）的左心室质量相关，但与血压正常者无关（r = 0.21，无统计学意义）。