Aldosterone

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.

Aldosterone deficiency adversely affects pregnancy outcome in mice

“…Aldosterone plays a central role in the long-term control of extracellular volume by adapting renal and extrarenal reabsorption of sodium to blood pressure [3]. Thereby, extracellular NaCl and volume is enlarged, blood pressure and organ dams had a feto-placental phenotype with decreased litter size, smaller placentas and fetuses, yet no overt preeclampsia.…”

Protein kinase D1 modulates aldosterone-induced ENaC activity in a renal cortical collecting duct cell line

“…The principal effect of aldosterone action in renal and colonic epithelia is in the regulation of membrane transport molecules, such as the epithelial sodium channel (ENaC). ENaC activity plays a crucial role in the maintenance of whole body Na+ homeostasis (1,2); the abundance of ENaC along the aldosterone-sensitive distal nephron (ASDN), coupled with channel trafficking into the apical membrane of the epithelial cells facilitates and determines the rate of Na+ re-absorption from the renal ultra-filtrate. The release of aldosterone as the last phase of the renin/ angiotensin cascade maintains tight hormonal control over ENaC expression and membrane insertion.…”

Aldosterone as a renal growth factor

“…The rennin-angiotensin-aldosterone system (RAAS) is a key regulator of systemic blood pressure through its direct action on the renal and cardiovascular systems [1,2]. The release of aldosterone by the adrenal glands contributes to the homeostatic regulation of blood pressure under normal physiological conditions via a number of interlinked mechanisms including the modulation of vascular tone and the rate of electrolyte transport across target epithelia such as the distal nephron.…”