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Am J Physiol Lung Cell Mol Physiol 276: L466-L473, 1999;
1040-0605/99 $5.00
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Vol. 276, Issue 3, L466-L473, March 1999

Nitric oxide-mediated regulation of transepithelial sodium and chloride transport in murine nasal epithelium

Heather L. Elmer1, Kristine G. Brady2, Mitchell L. Drumm1,2, and Thomas J. Kelley1,3

Departments of 1 Pediatrics and 3 Physiology and Biophysics and 2 Center for Human Genetics, Department of Genetics, Case Western Reserve University, Cleveland, Ohio 44106

Transepithelial ion transport is regulated by a variety of cellular factors. In light of recent evidence that nitric oxide (NO) production is decreased in cystic fibrosis airways, we examined the role of NO in regulating sodium and chloride transport in murine nasal epithelium. Acute intervention with the inducible NO synthase (iNOS)-selective inhibitor S-methylisothiourea resulted in an increase of amiloride-sensitive sodium absorption observed as a hyperpolarization of nasal transepithelial potential difference. Inhibition of iNOS expression with dexamethasone also hyperpolarized transepithelial potential difference, but only a portion of this increase proved to be amiloride sensitive. Chloride secretion was significantly inhibited in C57BL/6J mice by the addition of both S-methylisothiourea and dexamethasone. Mice lacking iNOS expression [NOS2(-/-)] also had a decreased chloride-secretory response compared with control mice. These data suggest that constitutive NO production likely plays some role in the downregulation of sodium absorption and leads to an increase in transepithelial chloride secretion.

cystic fibrosis; cystic fibrosis transmembrane conductance regulator; inducible nitric oxide synthase


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