Relation between the renin-angiotensin-aldosterone system and left ventricular structure and function in young normotensive and mildly hypertensive subjects

Abstract

Background: High angiotensin II levels in relation to the corresponding urinary sodium excretion have been found to modulate left ventricular (LV) structure in middle-aged hypertensive patients. To analyze whether such a relation between the renin-angiotensin-aldosterone system and left ventricular structure is already present in young individuals, we examined the changes of angiotensin II and aldosterone in response to increased salt intake and their relations to LV structure and function. Methods: In 119 young (aged 26 ± 3 years) patients with normal or mildly elevated blood pressure, we determined LV structure and function (2-dimensional guided M-mode echocardiography and pulse wave Doppler sonography) and 24-hour ambulatory blood pressure (SpaceLabs 90207). Dietary sodium intake as estimated by 24-hour urinary sodium excretion, plasma renin activity, angiotensin II, and aldosterone concentrations were measured first on a normal diet and second at high salt intake to determine the extent of the resulting suppression of the renin-angiotensin-aldosterone system. Results: Body mass index (r = 0.43, P < .001) and both systolic (r = 0.24, P < .01) and diastolic (r = 0.19, P < .05) 24-hour ambulatory blood pressure correlated with LV mass. No straightforward relation was found between LV structure and baseline angiotensin II or aldosterone concentration. The increase of sodium excretion at high salt intake was related to a physiologically expected decrease of angiotensin II and aldosterone levels in normotensive (r = –0.36, P < .01 and r = –0.32; P = .016, respectively) but not in hypertensive patients. Changes in angiotensin II or aldosterone concentration were not related to LV structure in either hypertensive or normotensive young individuals. However, changes in aldosterone secretion correlated with diastolic filling parameters in hypertensive patients (velocity-time integrals of the A over E wave: r = 0.32, P = .03; atrial contribution of LV filling: r = 0.33, P = .025) but not in normotensive individuals. Conclusion: In contrast to middle-aged hypertensive patients, neither angiotensin II, aldosterone, nor their suppression in response to high salt intake were related to LV structure in young hypertensive patients. However, inadequate suppression of aldosterone after salt intake was associated with diastolic filling abnormalities in our young hypertensive patients, which may represent early changes in hypertensive heart disease and precede potential structural alterations. (Am Heart J 1999;138:810-7.)