Prostaglandin E (PGE) has a cytoprotective role in the gastric parietal cell. PGE opened a housekeeping basolateral Cl channel of rabbit gastric parietal cells, the single channel conductance of which was about 0.3 picosiemens. In the present patch-clamp and Fura 2 fluorescence studies, we found that PGE increased the intracellular free Ca concentration ([Ca]) and that PGE-induced opening of the Cl channel depended on the increase in [Ca]. A novel bifunctional prostaglandin EP agonist/EP antagonist, 5(Z)-7-[(1S, 2S, 3S, 5R)-3-(trans--styren)sulfonamido-6,6-dimethylbicyclo(3.1.1)hept-2-yl]-5-heptenoic acid, also increased both [Ca] and channel opening. The PGE-induced effect was mediated via production of nitric oxide (NO); that is, N-monomethyl-L-arginine, an inhibitor of NO production, markedly inhibited the PGE-induced channel opening, and nitroprusside, a NO donor, induced the channel opening in the absence of PGE. Both PGE and A23187, a Ca ionophore, elevated the cGMP content of isolated parietal cells. The A23187-induced channel opening was abolished by methylene blue, a guanylate cyclase inhibitor. In conclusion, we found that the PGE-induced opening of the housekeeping Cl channel in the parietal cell involves the EP receptor-mediated increase in [Ca] via a pertussis toxin-sensitive GTP-binding protein, resulting in successive production of NO and cGMP.

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