Congestive heart failure (CHF) is characterized by activation of (i) vasopressor and antinatriuretic influences (ii) and by counter-activation of vasodilator natriuretic systems. The former comprise the sympathoadrenal, renin-angiotensin-aldosterone and arginine vasopressin systems, and possibly endothelin and withdrawal of endothelium dependent relaxing factor respectively. The latter include the prostaglandins (PGE-2, PGI-2), dopamine and atrial natriuretic factor. The response of the kidney to chronic heart failure, i.e. vasoconstriction and antinatriuresis, resembles the renal reaction to volume depletion. The adverse renal effects of ACE inhibitors in some patients with advanced congestive heart failure may be explained by lowering of renal perfusion pressure and dependence of glomerular filtration rate on angiotensin II.