[Aldosterone--classic and non classic effects].
Aldosterone, the major mineralocorticoid and most potent sodium retaining hormone in mammals was discovered in 1952 by Simpson and Tait. Since then numerous studies were carried out to explore the mechanisms underlying the biological actions of this steroid hormone, and the physiological effects of aldosterone remained an attractive area of research. The utilization of sophisticated molecular biology techniques led to the identification of genes encoding major components of the aldosterone-regulated sodium reabsorptive pathway, such as mineralocorticoid receptor. 11b-hydroxysteroid dehydrogenase type 2, epithelia Na+ channel, and sgk and Kras genes. It is clear that aberrations in these genes lead to genetic diseases affecting blood pressure and fluid homeostasis. However, in the last decade several clinical and experimental studies have implicated aldosterone in the pathogenesis of cardiovascular dysfunction, especially heart failure. In this context, aldosterone increases the accumulation of collagen in the fibroblast and myocytes of the cardiac tissue leading to fibrosis and cardiac hypertrophy. Blockade of aldosterone receptors by spironolactone substantially reduced the risk of morbidity and death among patients with severe heart failure. The present review summarizes the recent developments in the molecular mechanisms of aldosterone actions and its involvement in the pathogenesis of heart failure.
Department of Vascular Surgery and Kidney Transplantation, Rambam Medical Center, Haifa, Israel.
Tony
T
Karram
Aaron
A
Hoffman
Anan
A
Abbasi
Zaid
Z
Abassi
D000450:Aldosterone / Q000494:pharmacology / Q000502:physiology*; D006332:Cardiomegaly / Q000503:physiopathology; D003094:Collagen / Q000378:metabolism; D011905:Genes, ras; D006321:Heart / Q000502:physiology; D006801:Humans; D018482:Muscle, Skeletal / Q000502:physiology; D015222:Sodium Channels / Q000502:physiology
D015222:Sodium Channels; D000450:Aldosterone; D003094:Collagen