Despite large changes in water and salt intake, the kidney is able to maintain the extracellular osmolarity and volume within narrow margins (Verrey et al., 2000). Such fine control requires specific factors or hormones; among them, aldosterone and antidiuretic hormone (ADH) (vasopressin in mammals) play the key role. The main effector for the sodium balance is the epithelial sodium channel expressed in the apical membrane of the principal cell located in the distal nephron (distal convoluted tubule and collecting duct). The effect of aldosterone on sodium transport has been highly conserved throughout the evolution of vertebrates, whereas that of vasopressin varies from species to species. In the urinary bladder of the toad (Girardet et al., 1986) and in the cortical collecting duct (CCD) of the rat (Reif et al., 1986), ADH increases sodium transport through a cAMP-dependent mechanism, via...
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1 July 2002
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June 24 2002
Hormonal Regulation of the Epithelial Sodium Channel ENaC : N or Po?
Bernard C. Rossier
Bernard C. Rossier
Institute of Pharmacology and Toxicology, University of Lausanne, Lausanne CH-1005, Switzerland
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Bernard C. Rossier
Institute of Pharmacology and Toxicology, University of Lausanne, Lausanne CH-1005, Switzerland
Online ISSN: 1540-7748
Print ISSN: 0022-1295
The Rockefeller University Press
2002
J Gen Physiol (2002) 120 (1): 67–70.
Citation
Bernard C. Rossier; Hormonal Regulation of the Epithelial Sodium Channel ENaC : N or Po? . J Gen Physiol 1 July 2002; 120 (1): 67–70. doi: https://doi.org/10.1085/jgp.20028638
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