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Gastric mucosal endogenous prostanoids are involved in the cellular regulation of acid secretion from isolated parietal cells

A Choquet, R Magous and JP Bali

Laboratoire de Biochimie des Membranes, Institut National de la Sante et de la Recherche Medicale CJF 9207, Faculte de Pharmacie, Montpellier, France.

The effect of the cyclooxygenase inhibitor, indomethacin, was studied on histamine- and carbachol-induced [14C]aminopyrine (AP) accumulation in isolated rabbit gastric parietal cells. A 10-min preincubation period with 200 microM indomethacin enhanced AP accumulation caused by 0.1 mM histamine (3.5 x) or by 0.1 mM 3-isobutyl-1-methylxanthine (1.8 x), and this effect was reversed by addition of 10 microM misoprostol [a stable PG (prostaglandin)E1 analog]. This suggests that endogenous PGs from the E series are involved in the down regulation of histamine- induced AP accumulation. In contrast, the same preincubation of cells with 200 microM indomethacin reduced carbachol-stimulated AP accumulation and this inhibition was not reversed by adding misoprostol. Moreover, this inhibitory effect on carbachol-induced AP accumulation was enhanced (80% inhibition) after preincubation with indomethacin, suggesting that prostanoids other than PGs from the E series may also regulate carbachol-induced AP accumulation. This was supported by the fact that carbachol released PGE2 from parietal cells and that this release was blocked by pretreatment with indomethacin. We concluded that: 1) endogenous prostanoids down regulate histamine- stimulated acid secretion; 2) PGs from the E series inhibited carbachol- stimulated acid secretion; and 3) carbachol stimulated the production of PGE2 and probably of other prostanoids in parietal cells which in turn stimulated carbachol-induced acid secretion.

Volume 266, Issue 3, pp. 1306-1311, 09/01/1993
Copyright © 1993 by American Society for Pharmacology and Experimental Therapeutics




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Copyright © 1993 by the American Society for Pharmacology and Experimental Therapeutics.