Nephrol Dial Transplant (2003) 18: 1693-1695
© 2003 European Renal Association-European Dialysis and Transplant Association
Editorial Comment
Non-genomic actions of aldosterone: mechanisms and consequences in kidney cells
Department of Clinical Pharmacology, Faculty of Clinical Medicine Mannheim, Heidelberg University, Mannheim, Germany
Correspondence and offprint requests to: Martin Wehling, MD, Department of Clinical Pharmacology, Faculty of Clinical Medicine Mannheim, Heidelberg University, Theodor-Kutzer Ufer 1-3, D-68167 Mannheim, Germany. Email: martin.wehling@kpha.ma.uni-heidelberg.de
Keywords: aldosterone; early induced genes; kidney; non-genomic effects; renal disease
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Introduction
Steroid-hormone action in the classical sense means binding to intracellular receptors, binding of the hormonereceptor complex to DNA and activation or repression of transcription of target genes. However, all classes of steroid hormones can additionally act through non-genomic mechanisms and thereby change physiological processes [1]. In contrast to genomic steroid actions, these non-genomic effects are characterized with rapid onset and insensitivity towards inhibitors of transcription and translation. Non-genomic effects of aldosterone on various target organs and cells have been described, i.e. vascular smooth muscle cells and endothelial cells [2], skeletal muscle cells [3], lymphocytes [4], cardiac myocytes [5], colonic epithelial cells [6] and kidney cells [7]. In the classical target organ, the kidney, aldosterone stimulates Na+ (re)absorption and K+ secretion through both mechanisms, genomic as well as non-genomic [8].
Mechanisms involved in non-genomic aldosterone action
Crosstalk between non-genomic and genomic aldosterone actions
Aldosterone as a mediator of renal dysfunction
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