W. Rees, A. Garner, L.A. Turnberg
Aug 1, 1982
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Journal
Gastroenterology
Abstract
The effect of low concentrations of sodium taurocholate on the secretory and electrical activity of isolated rabbit fundic mucosa has been studied. Fundic mucosa maintained a stable potential difference (10.2 +/- 0.6 mV, n = 70) and electrical resistance (85 +/- 6 omega . cm-2, n = 70) and the majority of preparations spontaneously secreted acid (2.85 +/- 0.31 mumol . cm-2 . h-1, n = 70). Histamine (10(-5) and 10(-4) M) and carbachol (10-4 M) increased acid secretion, and these responses were prevented by cimetidine (10(-3) M) and atropine (10(-5) M), respectively. Mucosal application of taurocholate (10(-4) and 10(-3) M) increased net acidity without altering electrical activity. This response exhibited tachyphylaxis, was not altered by pretreating the tissues with cimetidine (10(-3) M), atropine (10(-5) M), or somatostatin (10(-6) M), and occurred in mucosas maximally stimulated by histamine. Sodium thiocyanate (6 x 10(-2) M, serosal side) inhibited spontaneous acid secretion revealing net alkalinization (0.83 +/- 0.05 mumol . cm-2 . h-1, n = 58) that was completely inhibited by anoxia and potassium cyanide (10(-2) M) and markedly reduced by 2,4-dinitrophenol (10(-4) M). Some fundic preparations spontaneously secreted alkali (1.20 +/- 0.20 mumol . cm-2 . h-1, n = 6) after an initial period of acid secretion. Mucosal-side taurocholate (10(-3) M) converted net alkali secretion by both thiocyanate-treated and spontaneously-secreting mucosas to acid secretion without affecting electrical conductance. These secretory responses may be implicated in the pathogenesis of gastric mucosal damage by bile salts.