Contrary to popular belief, the primary directive for the release of renin is not the preservation of circulatory homeostasis, since activation of this hormonal system in patients with chronic heart failure results in deleterious rather than beneficial effects on cardiac performance. Instead, renin appears to be released by the kidneys to maintain glomerular filtration rate when renal perfusion pressure is reduced. The renin-angiotensin system carries out this beneficial action by exerting a constrictor action on the efferent arteriole. In doing so, renal blood flow declines, but filtration fraction increases and thus, glomerular hydraulic filtration pressure (and renal function) is preserved, despite severe renal hypoperfusion. When the formation of angiotensin II is inhibited during converting-enzyme inhibition, the beneficial action of this hormone on the efferent arteriole is lost, and renal function may deteriorate. This sequence of events is most likely to be seen when four risk factors are present: hyponatremia; high-dose diuretic therapy; diabetes mellitus; and the use of long-acting converting-enzyme inhibitors. In randomized studies, renal insufficiency developed more frequently with enalapril and lisinopril than with captopril. This risk of worsening azotemia is particularly high in patients with the most severe (class IV) heart failure.