in experimental studies, the importance of aldosterone for the development of left ventricular (LV) hypertrophy has been demonstrated. In 120 healthy Caucasian men (aged 25 +/- 3 years; blood pressure, 134 +/- 15/86 +/- 12 mm Hg), we determined LV mass (2-climensionally guided Mmode echocardiography), urinary aldosterone concentration, and the response of aldosterone to angiotensin II infusion (3.0 ng/kg/min). Seventy-six volunteers took part in a follow-up visit after 2 years when urinary aldosterone concentration and LV mass were determined again. At follow-up, LV mass increased in 42 subjects (by 33 26 g), whereas in 34 subjects LV mass decreased (by 27 22 g). Between the 2 groups, only the change in urinary aldosterone concentration over time was significantly different (group with increased LV mass had an increase in urinary aldosterone concentration by 2.5 +/- 5.4 mug/day; group with decreased LV mass had a decrease in urinary aldosterone concentration by 0.7 +/- 4.6; p < 0.01 between groups). In accordance, we found significant correlations between changes in LV mass and changes in urinary aldosterone concentration (r = 0.29, p < 0.05) and between changes in LV mass and the response of aldosterone to angiotensin 11 at baseline (r = 0.25, p < 0.05). Both changes in aldosterone concentration over time and the response of aldosterone to angiotensin II were related to changes in LV mass over time. These data underscore the importance of aldosterone for the development of LV hr pertrophy. This process is already evident in young subjects with apparently small changes in LV mass over a mean follow-up period of 2 years. (C) 2003 by Excerpta Medica, Inc.