Control of renal perfusion and function in congestive heart failure.
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.
Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115.
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Hollenberg
D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D000818:Animals; D001794:Blood Pressure; D001810:Blood Volume; D001834:Body Water / Q000378:metabolism; D005919:Glomerular Filtration Rate; D006333:Heart Failure / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology*; D006801:Humans; D007668:Kidney / Q000378:metabolism / Q000503:physiopathology*; D008274:Magnesium / Q000378:metabolism; D011188:Potassium / Q000378:metabolism; D012079:Renal Circulation; D012964:Sodium / Q000378:metabolism; D014661:Vasoconstriction
D000806:Angiotensin-Converting Enzyme Inhibitors; D012964:Sodium; D008274:Magnesium; D011188:Potassium