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Institut National de la Santé et de la Recherche Médicale U-478, Faculté de Médecine X. Bichat-Institut Fédératif de Recherches 02, 75870 Paris Cedex 18, France
Aldosterone
regulates renal sodium reabsorption through binding to the
mineralocorticoid receptor (MR). Because the glucocorticoid receptor
(GR) is expressed together with the MR in aldosterone target cells,
glucocorticoid hormones bound to GR may also intervene to modulate
physiological functions in these cells. In addition, each steroid can
bind both receptors, and the MR has equal affinity for aldosterone and
glucocorticoid hormones. Several cellular and molecular mechanisms
intervene to allow specific aldosterone regulatory effects, despite the
large prevalence of glucocorticoid hormones in the plasma. They include
the local metabolism of the glucocorticoid hormones into inactive
derivatives by the enzyme 11
-hydroxysteroid dehydrogenase; the
intrinsic properties of the MR that discriminate between ligands
through differential contacts; the possibility of forming homo- or
heterodimers between MR and GR, leading to differential transactivation
properties; and the interactions of MR and GR with other regulatory
transcription factors. The relative contribution of each of these
successive mechanisms may vary among aldosterone target cells
(epithelial vs. nonepithelial) and according to the hormonal context.
All these phenomena allow fine tuning of cellular functions depending on the degree of cooperation between corticosteroid hormones and other
factors (hormonal or tissue specific). Such interactions may be altered
in pathophysiological situations.
aldosterone; glucocorticoid hormones; corticosteroid receptors; kidney; 11-hydroxysteroid dehydrogenase; sodium transport
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