Aldosterone is implicated in the pathogenesis of edema in congestive heart failure through mechanisms involving reduced renal blood flow, renin release, and elevated venous pressure.
The role of the adrenal in the pathogenesis of the edema of congestive heart failure has been debated for many years. Deming and Luetscher1in 1950 showed that the urine of patients with congestive failure contained a substance promoting sodium retention. This substance was subsequently identified by Simpson, Tait, Luetscher, and others to be aldosterone, and has been found in elevated amounts in the urine of patients with congestive heart failure by many investigators.2-5It has been postulated that the reduced renal blood flow secondary to lowered cardiac output in congestive failure leads to release of renin and enzymatic conversion of plasma factors to angiotensin II and stimulation of aldosterone secretion.6Another possible mechanism of the hyperaldosteronuria begins with elevated venous pressure and transudation of fluid and electrolytes from the vascular system. This is postulated to stimulate the production of aldosterone by way of as yet unelucidated
Louis L. Sanders (Sun,) conducted a review in Congestive heart failure. Aldosterone was evaluated. Aldosterone is implicated in the pathogenesis of edema in congestive heart failure through mechanisms involving reduced renal blood flow, renin release, and elevated venous pressure.