Abstract
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.
Keywords
AldosteroneHeart failureInternal medicineMedicineHyperaldosteronismCardiologyMineralocorticoid receptorEndocrinologyHomeostasisMineralocorticoidHormoneSpironolactoneEplerenone
MeSH Terms
AldosteroneAngiotensin-Converting Enzyme InhibitorsAnimalsDiureticsHeart FailureHumansMineralocorticoid Receptor AntagonistsReceptorsMineralocorticoidRenin-Angiotensin SystemSpironolactone
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Publication Info
- Year
- 1993
- Type
- review
- Volume
- 71
- Issue
- 3
- Pages
- A3-A11
- Citations
- 107
- Access
- Closed
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Cite This
Karl T. Weber,
Daniel Villarreal
(1993).
Aldosterone and antialdosterone therapy in congestive heart failure.
The American Journal of Cardiology
, 71
(3)
, A3-A11.
https://doi.org/10.1016/0002-9149(93)90238-8
Identifiers
- DOI
- 10.1016/0002-9149(93)90238-8
- PMID
- 8422002