Angiotensin II stimulates left ventricular hypertrophy in hypertensive patients independently of blood pressure

Angiotensin II (AII) is known to be a growth stimulating factor for myocard ial cells. We examined whether an exaggerated responsiveness to AII might a ggravate left ventricular (LV) hypertrophy in;human essential hypertension. To determine the responsiveness to All in humans, we examined changes in m ean arterial pressure (MAP), renal blood now (RBF), and glomerular filtrati on rate (GFR) (steady state input clearance technique with para-aminohippur ate and inulin, respectively) and aldosterone secretion to AII infusions (0 .5 and 3.0 ng/kg/min) in 71 normotensive male and 48 hypertensive male subj ects (age: 26 +/- 3 years; 24-h ambulatory blood pressure: 121 +/- 5/71 +/- 4 mmHg v 138 +/- 7/82 +/- 7 mmHg, P < .001). In addition, each patient und erwent two-dimensional guided M-mode echocardiography at rest to assess car diac structure and function. When given AII 3.0, a greater increase of MAP (13 +/- 7 v 17 +/- 8 mm Hg, P < .022) and a more marked decrease of RBF (-2 03 +/- 123 mL/min v -270 +/- 137 mL/min, P < .007) were found in hypertensi ves than in normotensives, whereas changes in GFR and aldosterone concentra tion were similar in both groups. Most important, changes in GFR to AII cor related with echocardiographically determined LV mass (normotensives: AII 0 .5: r = 0.33, P <.006, AII 3.0: r = 0.28, P < .05; hypertensives: AII 0.5: r = 0.41, P <.006, AII 3.0: r = 0.32, P < .05). After taking baseline MAP a nd body mass index into account, the increase in GFR to AII 0.5 in hyperten sives still correlated with EV mass (partial r = 0.37, P < .01). Inasmuch a s the increase of GFR is a marker of the responsiveness to AII (related to vasoconstriction at;the postglomerular site), our data suggest that increas ed sensitivity to AII is linked to LV hypertrophy in early essential hypert ension, independently of the level of blood pressure. (C) 1999 American Jou rnal of Hypertension, Ltd.