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 P(Glo) 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.
RCT Entities:
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 P(Glo) 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.
Authors: Christian Ott; Markus P Schneider; Ulrike Raff; Martin Ritt; Kristina Striepe; Marco Alberici; Roland E Schmieder Journal: Br J Clin Pharmacol Date: 2013-01 Impact factor: 4.335