Control of renal perfusion and function in congestive heart failure #MMPMID3414540
Hollenberg NK
Am J Cardiol 1988[Sep]; 62 (8): 72E-75E PMID3414540show ga
The force that shaped the evolution of the kidney, anatomically and functionally, has been defense of extracellular fluid volume. Similarly, the role of the renin-angiotensin-aldosterone system in normal physiology involves volume homeostasis rather than blood pressure control. When a volume deficit occurs, e.g., by restriction of sodium intake or through hemorrhage, a substantial part of the renal vasoconstriction that occurs is due to angiotensin II. In this context, the renal response to congestive heart failure resembles the response to a volume deficit, with angiotensin-mediated renal vasoconstriction contributing to the decrease in blood flow, glomerular filtration rate and to sodium retention. Thus, converting-enzyme inhibition improves renal perfusion and function, including sodium, potassium, magnesium and water handling, as a major part of its therapeutic contribution in congestive heart failure.
Am+J+Cardiol 1988 ; 62 (8): 72E-75E
