PMID: 9543596Apr 17, 1998Paper

Inadequate suppression of angiotensin II modulates left ventricular structure in humans

Clinical Nephrology
M P SchlaichR E Schmieder

Abstract

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. 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. 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 base...Continue Reading

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