Aldosterone and antialdosterone therapy in congestive heart failure.
The pathophysiologic cycle that links myocardial failure with the appearance of congestive heart failure is not fully understood. It is clear, however, that an activation of several neurohormonal systems and the interplay between kidneys, adrenal glands, and heart contribute to abnormal sodium and water homeostasis. Aldosterone, the body's most potent mineralocorticoid hormone, contributes to intravascular and extravascular volume expansion, and thus to the appearance of symptomatic failure. Antialdosterone therapy in patients with secondary hyperaldosteronism due to heart failure must achieve one or more of the following goals: reduce or, preferably, normalize plasma aldosterone levels by limiting synthesis; antagonize the renal and systemic effects of aldosterone at its receptor sites; and eliminate or minimize the multiple stimuli to aldosterone secretion.
Weber
K T
KT
Department of Internal Medicine, University of Missouri, Columbia 65212.
Villarreal
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D
D000450:Aldosterone / Q000502:physiology*; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D000818:Animals; D004232:Diuretics / Q000627:therapeutic use; D006333:Heart Failure / Q000188:drug therapy* / Q000503:physiopathology*; D006801:Humans; D000451:Mineralocorticoid Receptor Antagonists / Q000627:therapeutic use*; D018161:Receptors, Mineralocorticoid / Q000187:drug effects; D012084:Renin-Angiotensin System / Q000187:drug effects / Q000502:physiology; D013148:Spironolactone / Q000627:therapeutic use
D000806:Angiotensin-Converting Enzyme Inhibitors; D004232:Diuretics; D000451:Mineralocorticoid Receptor Antagonists; D018161:Receptors, Mineralocorticoid; D013148:Spironolactone; D000450:Aldosterone