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.