Background: To elucidate the renoprotective mechanism of AT(1)-receptor blockers, we compared the effects of the AT(1)-receptor blocker valsartan- with those of the calcium channel blocker amlodipine on renal hemodynamics and microcirculation. Methods: A total of 58 patients (50.2 +/- 9.0 years) with mild to moderate essential hypertension were included in a randomized, double-blind study to receive either valsartan (80 to 160 mg) or amlodipine (5 to 10 mg). Renal plasma flow (RPF) and glomerular filtration rate (GFR) were measured before and after 8 weeks of treatment. Glomerular hydrostatic pressure (P-Glo) and resistances of the afferent (R-A) and efferent (R-E) arterioles were calculated according to the Gomez formulas. Results: Blood pressure control was similar in both groups. RPF did not change with either treatment. In contrast, GFR increased with amlodipine (+8 +/- 14 mL/min; P < .01) but was preserved with valsartan. Amlodipine caused a more marked increase in the R-E/R-A ratio than valsartan (+0.26 +/- 0.26 v +0.13 +/- 0.24, P < .05), which was paralleled by an increase in PGlo in patients treated with amlodipine (+ 1.9 +/- 4.3 mm Hg; P < .05) but not in those treated with valsartan. Conclusions: At similar blood pressure control, valsartan maintained GFR and P-Glo, whereas amlodipine led to glomerular hyperfiltration and an increase in P-Glo. The results might explain the favorable renal outcome with AT(1)-receptor blocker therapy. (C) 2003 American Journal of Hypertension, Ltd.