A considerable number of hormones control renal perfusion to preserve glomerular filtration. We used the "captopril test" to characterize patients with renal-vascular hypertension. This study revealed a group of patients which reacted to 25 mg of captopril with a significant increase of plasma renin activity, but angiography excluded a renal artery stenosis. These patients had significantly more hypertensive organ damage than a control-group, including a significant microalbuminuria. Consequently, we infused a subpressure dose of angiotensin II to investigate its impact on albuminuria in these patients. Although angiotensin II induced hyperfiltration, microalbuminuria was not increased. Because this finding could have therapeutic relevance, we investigated the significance of different antihypertensive drugs (beta-blocker, alpha-blocker, Calcium antagonists, ACE-inhibitor) on microalbuminuria in patients with arterial hypertension. Renal hemodynamics were influenced as expected, but blood-pressure and microalbuminuria were reduced to the same extent by all antihypertensives. In contrast to these results, we could demonstrate significantly different influences of a beta-blocker and an ACE-inhibitor on proteinuria in patients with primary glomerulonephritis. These results suggest different effects of antihypertensive drugs on renal protein excretion depending on the actual disease.