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Am J Physiol Lung Cell Mol Physiol 281: L450-L457, 2001;
1040-0605/01 $5.00
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Vol. 281, Issue 2, L450-L457, August 2001

Regulation of anion secretion by nitric oxide in human airway epithelial cells

Marek Duszyk

Department of Physiology, University of Alberta, Edmonton, Alberta T6G 2H7, Canada

Nitric oxide (NO) is continuously produced and released in human airways, but the biological significance of this process is unknown. In this study, we have used Calu-3 cells to investigate the effects of NO on transepithelial anion secretion. An inhibitor of NO synthase, NG-nitro-L-arginine methyl ester, reduced short- circuit current (Isc), whereas an NO donor, S-nitrosoglutathione (GSNO), increased Isc, with an EC50 ~1.2 µM. The NO-activated current was inhibited by diphenylamine-2-carboxylate, clotrimazole, and charybdotoxin. Selective permeabilization of cell membranes indicated that NO activated both apical anion channels and basolateral potassium channels. An inhibitor of soluble guanylate cyclase, 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one, prevented activation of Isc by NO but not by 8-bromo-cGMP, suggesting that NO acts via a cGMP-dependent pathway. Sequential treatment of cells with forskolin and GSNO or 1-ethyl-2-benzimidazolinone and GSNO showed additive effects of these chemicals on Isc. Interestingly, GSNO elevated intracellular Ca2+ concentration ([Ca2+]i) but had no effect on Isc activated by thapsigargin. These results show that NO activates transepithelial anion secretion via a cGMP-dependent pathway that involves cross talk between NO and [Ca2+]i.

Calu-3 cells; guanosine 3'5'-cyclic monophosphate; chloride channels; potassium channels


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