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AJP - Gastrointestinal and Liver Physiology, Vol 264, Issue 1 51-G56, Copyright © 1993 by American Physiological Society
ARTICLES |
A. K. Sandvik, E. Brenna and H. L. Waldum
Department of Medicine, University Hospital, Trondheim, Norway.
This study examined the second messenger system responsible for gastrin-induced histamine release from the rat stomach. We examined the effect of different concentrations of ionized calcium, the calcium-channel blockers verapamil and nicardipine, and the intracellular calcium-chelator 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid/acetoxymethyl ester (BAPTA/AM) on gastrin-stimulated histamine release in the totally isolated vascularly perfused rat stomach. Moreover, the effect on baseline histamine release of caffeine as well as of forskolin and 3-isobutyl-1-methylxanthine (IBMX) was tested. Gastrin induced an immediate 10- to 15-fold increase in venous histamine. Perfusate ionized calcium in the 0.25-1.25 mM range did not affect histamine release; histamine release was attenuated by the 0.00 and 1.75 mM calcium concentrations. Verapamil, nicardipine, and BAPTA/AM inhibited gastrin-stimulated histamine release. Caffeine stimulated the release, whereas forskolin and IBMX had no effect. We conclude that gastrin-induced histamine release from the rat stomach is mediated by calcium, probably both from the intracellular pool and by transmembrane flux from the extracellular space.
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