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1 Department of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, CT, USA
* To whom correspondence should be addressed. E-mail: cecilia.canessa{at}yale.edu.
The increase in epithelium sodium channel (ENaC) activity induced by aldosterone in the distal tubule of the kidney has been attributed to sgk1 (serum and glucocorticoid induced kinase). The distal colon constitutes another classical aldosterone-responsive epithelium that expresses both ENaC and sgk1 in an aldosterone-dependent manner. However, the site of expression and the temporal relation of the aldosterone induction of these two proteins have not been investigated. Here, we examined the distribution and abundance of sgk1 in the rat intestine under basal conditions and after changes in the concentration of aldosterone and glucocorticoids. The results indicate that sgk1 is expressed in the distal colon and also in the ileum and jejunum. The abundance of sgk1 was high in control animals and it did not change significantly after induction of sodium depletion or after a single dose of aldosterone whereas it decreased after adrenalectomy. In contrast the three subunits of ENaC were markedly induced in the distal colon by acute and chronic increases in aldosterone levels. The results indicate differential regulation of sgk and ENaC subunits by aldosterone in the distal colon. The distribution of sgk1 in the intestine beyond the aldosterone-responsive segments suggests that sgk1 may regulate in addition other sodium transporters in the intestinal epithelium.
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