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Advan. Physiol. Edu. 26: 8-20, 2002;
1043-4046/02 $5.00
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ADV PHYSIOL EDUC 26:8-20, 2002
© 2002 American Physiological Society

STAYING CURRENT

ALDOSTERONE

Rachell E. Booth1, John P. Johnson2 and James D. Stockand1

1 Department of Physiology, University of Texas Health Science Center San Antonio, San Antonio, Texas 78229
2 Department of Medicine, Renal-Electrolyte Division, University of Pittsburgh, Pittsburgh, Pennsylvania 15213

Abstract

Aldosterone plays a pivotal role in electrolyte and fluid homeostasis and thus control of blood pressure. The "classical" view of aldosterone action is that it targets epithelia of the distal colon and renal nephron to stimulate Na+ (re)absorption and K+ secretion. In these cells, aldosterone binds steroid receptors, promoting translocation to the nucleus, where they modulate gene expression with the induced proteins stimulating transport. This "genomic" action is dependent on transcription and translation and has a latency of 0.5–1.0 h. Recently, more rapid actions of aldosterone that are independent of transcription and translation have been described. These "nongenomic" actions are mediated by a distinct receptor that is insensitive to inhibitors of the classical mineralocorticoid receptor, such as spironolactone. The present review describes advances in our understanding of the classical model of aldosterone action as well as those that broaden this model to encompass nongenomic actions, nonepithelial targets, production of aldosterone outside of the adrenal gland, novel mechanisms of specificity, and novel mechanisms for mediating genomic actions.

Key words: epithelial Na+ channel; serum and glucocorticoid-inducible kinase; Ras; blood pressure; epithelia




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