In congestive heart failure renal hemodynamics are characterized by a decrease of fractional renal blood flow (renal fraction of the cardiac output) and marked changes of the intrarenal circulation. The latter consists of cortical hypocirculation and an enhanced medullary blood flow in the presence of a relative rise in glomerular filtration rate (GFR). This compensatory increment of GFR is mediated by a stimulation of prostaglandins (dilatation of vas afferens) as well as the renin-angiotensin- and adrenergic systems (contraction of vas efferens). Therapy with ACE inhibitors influences renal function in a complex manner. A decline in GFR resulting in the worst case in acute renal failure (ARF) may be caused by two pathogenetic possibilities: 1. critical reduction in renal perfusion pressure (below 70 mm Hg) and/or 2. loss of the autoregulation of GFR by relaxation of the constricted vas efferens induced by stimulation of the renin-angiotensin-systems (RAS). Activation of the RAS might be a consequence of severe renal hypocirculation as well as a diuretic induced volume and sodium depletion (contraction of the effective arterial blood volume). On the other hand, ACE inhibitors may improve renal blood flow and glomerular filtration rate. This may be due to a rise in cardiac output, dilatation of vas efferens and occasionally vas afferens and an increase of the ultrafiltration coefficient. The deterioration of renal function caused by ACE-inhibitors may be prevented by avoiding a volume and sodium deficit (withdrawal or reduction of diuretics) and careful titration of the ACE-inhibitor starting with lowest dosages.