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Am J Physiol Lung Cell Mol Physiol 274: L990-L996, 1998;
1040-0605/98 $5.00
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Vol. 274, Issue 6, L990-L996, June 1998

Regulation of amiloride-sensitive sodium absorption in murine airway epithelium by C-type natriuretic peptide

Thomas J. Kelley1, Calvin U. Cotton1, and Mitchell L. Drumm1,2

1 Department of Pediatrics and 2 Department of Genetics, Center for Human Genetics, Case Western Reserve University, Cleveland, Ohio 44106-4948

We have previously shown that C-type natriuretic peptide (CNP), a guanylate cyclase agonist, can stimulate cystic fibrosis transmembrane conductance regulator (CFTR)-mediated chloride secretion in murine airway epithelial cells via protein kinase (PK) A activation through the inhibition of cGMP-inhibited phosphodiesterases. In this paper, we show that CNP is also capable of reducing amiloride-sensitive sodium absorption in murine airway epithelium through a cGMP-dependent mechanism that is separate from the CFTR regulatory signaling pathway. Both murine tracheal and nasal tissues exhibit sensitivity to amiloride-sensitive sodium regulation by exogenously added CNP. CNP depolarized the nasal transepithelial potential difference by 6.3 ± 0.5 mV, whereas the cGMP-inhibited phosphodiesterase inhibitor milrinone actually hyperpolarized the nasal transepithelial potential difference by 2.0 ± 1.2 mV in mice homozygous for a CFTR stop mutation [CFTR(-/-)]. Inhibition of guanylate cyclase activity and PKG activity in normal mice resulted in an increase in amiloride-sensitive sodium absorption, suggesting that tonic regulation of amiloride-sensitive sodium absorption is in part due to basal cGMP levels and PKG activity.

guanylate cyclase; guanosine 3',5'-cyclic monophosphate


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