Inadequate suppression of angiotensin II modulates left ventricular structure in humans

Background: In a previous study we found that high angiotensin II levels in relation to the corresponding urinary sodium excretion aggravate left vent ricular hypertrophy in hypertensive patients. To analyze whether a dysregul ation of the renin-angiotensin-aldosterone system determines left ventricul ar structure in young individuals, we examined whether the response of angi otensin II after increasing salt intake is related to left ventricular stru cture. Methods: In 51 young, male Caucasians with normal or mildly elevated blood pressure, left ventricular structure, 24-hour ambulatory blood press ure and dietary sodium intake las estimated by 24-hour sodium excretion) we re determined in parallel with plasma renin activity, angiotensin II, and a ldosterone concentrations. Angiotensin II concentration and 24-hour sodium excretion were measured twice: firstly on a normal Bavarian diet and second ly at high salt intake to determine the resulting suppression of the renin- angiotensin-aldosterone system. Results: Body mass index (r = 0.42, p < 0.0 01) and both systolic (r = 0.28, p < 0.05) and diastolic (r = 0.25, p < 0.0 5) 24-hour ambulatory blood pressure correlated with left ventricular mass. No direct relationship was found between left ventricular structure and ba seline angiotensin II concentration. The lower the physiological decrease o f angiotensin II after high oral salt intake, i.e. the higher the angiotens in II level after salt intake remained, the greater was left ventricular ma ss (r = 0.38, p < 0.006) even after taking 24-hour ambulatory blood pressur e into account (partial correlation; r = 0.43, p < 0.005). Consistently, an giotensin II concentration at high salt intake correlated with left ventric ular 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 I I levels in normotensive (r = -0.43, p < 0.05), but not in hypertensive sub jects (r = 0.16, n.s.). The changes in angiotensin II concentration at high salt intake were related to left ventricular mass in hypertensive (r = 0.4 3, p < 0.02), but not in normotensive individuals (r = 0.21, n.s.. Conclusi on: Our finding that angiotensin II concentration at high salt intake corre lated with left ventricular mass independently of ambulatory blood pressure suggests that inadequate suppression of angiotensin II after high salt int ake contributes to left ventricular hypertrophy already in young hypertensi ve individuals independently of blood pressure.