ACE-inhibitors are known to have special renal effects, i.e. they increase ERPF, decrease the filtration fraction and lower
proteinuria. These effects can be due to a decrease in
angiotensin II (AII) levels as well as an increase in
bradykinin. New and more specific AII-receptor antagonists may help to distinguish between effects exerted by
angiotensin II and those exerted by
bradykinin. We investigated the effects of
losartan in 9 patients with
essential hypertension (sitting mean diastolic blood pressure 95-120 mmHg). Renal hemodynamics were measured by continuous
inulin-and PAH-clearance (GFR and RPF) after stopping
antihypertensive therapy for 1 week, followed by a 2-week placebo period and after a 4-week treatment phase with
losartan (50 mg/die) followed by a
therapy with an
ACE-inhibitor (
ramipril 5mg/die). Additionally, urine
albumin excretion (UAE) was measured. Treatment of patients with
essential hypertension with
losartan resulted in a significant decrease of MAP after three weeks of treatment (121 +/- 8 mmHg under placebo and 114 +/- 10 mmHg under
losartan; * = p < 0.05). MAP after four weeks of
losartan treatment was 115 +/- 11 mmHg. Regarding changes in renal hemodynamics we could not demonstrate a significant change for neither
losartan nor the
ACE-inhibitor. Urine
albumin excretion was reduced by both treatment regimens in correlation to the magnitude of blood pressure reduction. Our data indicate that
losartan induced a significant reduction in MAP in patients with essential arterial
hypertension with only moderate effects on renal hemodynamics.