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 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.