Prince Henry’s Institute of Medical Research, Clayton, Victoria 3168, Australia
Correspondence: Address all correspondence and requests for reprints to: John W. Funder, Prince Henry’s Institute of Medical Research, P.O. Box 5152, Clayton, Victoria 3168, Australia. E-mail: john.funder{at}phimr.monash.edu.au
Aldosterone has physiological effects to regulate fluid andelectrolyte homeostasis across epithelia and proinflammatoryeffects on a variety of nonepithelial cells in the context ofinappropriate salt status. These effects are mediated by mineralocorticoidreceptors, members of a large family of nuclear transcriptionfactors, by DNA-directed, RNA-mediated protein synthesis. Rapideffects of aldosterone, insensitive to actinomycin D or cycloheximideand thus clearly nongenomic, have been convincingly documentedin a variety of epithelial and nonepithelial tissues. Despitestrenuous attempts, isolation of a nonclassical membrane receptorfor aldosterone has proven unsuccessful, and rapid nongenomiceffects mediated by classical mineralocorticoid receptors areincreasingly recognized in the kidney, heart, and vascular wall.The mechanism of rapid nongenomic actions of aldosterone mayvary between tissues in terms of pathways; in addition, whatremains to be established is the physiological role of aldosteroneaction via such rapid nongenomic mechanisms and how they mightsynergize with the longer time course genomic actions of mineralocorticoids.
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