The effects of non-steroidal anti-inflammatory drugs and prostaglandins E2 and F2α on the secretory and electrical activity of isolated rabbit fundic mucosa have been studied. Spontaneous acid secretion was inhibited by serosal side application of sodium thiocyanate (6×10−2M) and the resulting alkali secretion measured by pH stat tiration. Serosal side application of indomethacin (10−5M) or aspirin (3×10−3M) inhibited alkali secretion (0·55±0·06 to 0·12±0·06 μmol/cm2/h, n=6, p<0·01 and 0·28±0·06 to 0·11±0·03 μmol/cm2/h, n=7, p<0·02 respectively). Mucosal or serosal side prostaglandin E2 (10−5 to 10−10M) and F2α (10−4 to 10−10M) failed to alter the rate of alkalinisation but secretion was significantly increased by serosal side 16,16-dimethyl-prostaglandin E2 (10−6M) (0·90±0·20 to 1·50±0·30 μmol/cm2/h, n=6, p<0·01). Serosal side application of 10−6M prostaglandin E2 to fundic mucosae pretreated with either aspirin (5×10−3M) or indomethacin (10−5M), to reduce endogenous E2 formation, also failed to alter alkali secretion. Pretreatment of the mucosa with 16,16-dimethyl-E2 (10−6M) abolished the inhibitory effect of indomethacin (10−5M) on alkali secretion (n=6) but did not modify the secretory response to aspirin (3×10−3M) (fall in alkali secretion with aspirin = 81±11% and with aspirin plus 16,16-dimethyl-E2 = 72±10%, n=7). In the doses used, none of the prostaglandins or non-steroidal anti-inflammatory drugs altered transmucosal potential difference or electrical resistance. These results show that the damaging agents, aspirin and indomethacin, both inhibit gastric alkali secretion but that modes of action may differ. The observation that prostaglandins, E2 and F2α failed to increase alkali production suggests that their protective activity against a variety of damaging agents as shown by others, may be mediated by another mechanism.
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