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Am J Physiol Lung Cell Mol Physiol 274: L244-L251, 1998;
1040-0605/98 $5.00
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Vol. 274, Issue 2, L244-L251, February 1998

Evidence for functional ANP receptors in cultured alveolar type II cells

Pierre-Louis Tharaux1,2, Jean-Claude Dussaule1,2, Sylvianne Couette3,4, and Christine Clerici3,4

1 Institut National de la Santé et de la Recherche Médicale Unité 64, Hôpital Tenon, 75020 Paris; 2 Laboratoire de Physiologie Faculté Saint Antoine, 75012 Paris; 3 Institut National de la Santé et de la Recherche Médicale Unité 426, Faculté Xavier Bichat, 75018 Paris; and 4 Laboratoire de Physiologie, Faculté Léonard de Vinci, 93000 Bobigny, France

Because atrial natriuretic peptide (ANP) is considered to play a role in lung physiology and pathology, our aim was to characterize natriuretic peptide receptors in cultured rat alveolar type II (ATII) cells. Guanylate cyclase A- and B-receptor but not clearance-receptor mRNAs were detected by reverse transcription-polymerase chain reaction. The absence of clearance-receptor expression in ATII cells was confirmed by competitive inhibition of ANP binding; ANP (0.1-100 nM) decreased the binding of 125I-ANP, whereas C-ANP-(4---23), a specific ligand of clearance receptors, was ineffective. ANP induced a dose-dependent increase in guanosine 3',5'-cyclic monophosphate (cGMP) production, with a threshold of 0.1 nM, whereas the response to C-type natriuretic peptide was weak and was observed only at high concentrations (100 nM). In ATII cells cultured on filters, 1) ANP receptors were present on both the apical and basolateral surfaces and 2) cGMP egression was polarized, as indicated by the greater ANP-induced cGMP accumulation in the basolateral medium, and was partially inhibited by probenecid, an organic acid transport inhibitor. Influx studies demonstrated that ANP decreased the amiloride-sensitive component of 22Na influx but did not change ouabain-sensitive 86Rb influx. In conclusion, ATII cells behave as a target for ANP. ANP activation of guanylate cyclase A receptors produces cGMP, which is preferentially extruded on the basolateral side of the cells and inhibits the amiloride-sensitive Na-channel activity.

atrial natriuretic peptide; guanosine 3',5'-cyclic monophosphate; cyclic nucleotide export; amiloride-sensitive sodium-22 influx


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