Fluid retention in congestive heart failure may be driven by early increases in renal sympathetic activity and baroreceptor-mediated aldosterone secretion.
As a more detailed picture of the pathogenesis of salt and water retention in congestive heart failure evolves, it appears that increased tubular reabsorption of sodium occurs very early in heart disease, with further enhancement of the fluid accumulation as filtration rate decreases later in the disease process. Increase in sympathetic activity in the kidney can be demonstrated before the development of frank failure, and probably is initiated reflexly by decreased baroreceptor activity, a response that occurs in various types of circulatory insufficiency. Blocking the adrenergic nerves of the kidney produces profound diuresis and natriuresis. Evidence is presented that the pressoreceptors may also play an important role in regulating aldosterone secretion. Thus, the change in body fluids seen in congestive heart failure may be part of the normal reflex adjustments maintaining blood pressure.
A. C. Barger (Fri,) studied this question.