Stimulated Pepsin Secretion after Omeprazole-Induced Acid Suppression in the Totally Isolated, Vascularly Perfused Rat Stomach

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Abstract
The effect of the H2 agonist impromidine, gastrin 1-17 (G1-17), pentagastrin, and the M1 agonist McN-A-343 on pepsin secretion in the acid-inhibited totally isolated, vascularly perfused rat stomach was studied. Omeprazole produced a 97-98% inhibition of stimulated acid outputs. Base-line pepsin output after omeprazole was 712±278 µg/h (mean ± SEM) and, after stimulation with impromidine, 1528 ± 164 µg/h; Gl-17, 1520 ± 180 µg/h; and pentagastrin, 2063 ± 605 µg/h. Output after McN-A-343 was 534 ± 69 µg/h. Pepsin secretion after impromidine, G1-17, and pentagastrin was significantly (p < 0.01) higher than base-line output. McN-A-343 had no significant effect on pepsin output in this model. Pepsin secretion after impromidine, G1-17, and pentagastrin was considerably lower than found in the same model with uninhibited acid output. This could be caused by decreased tubular washout' after acid inhibition, and, accordingly, no conclusions can be drawn as to the possible stimulatory effect of acid on pepsin secretion. However, the present study indicates that pepsin secretion can be stimulated directly by impromidine and (penta)gastrin without concomitant acidification of the gastric glands.

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