A comparison of the effects of prostacyclin and the 15(S), 15-methyl analogs of PGE2 and PGF2-alpha on gastric parietal and nonparietal secretion.

Abstract

The mechanism by which prostaglandins protect the gastric mucosa is unclear. Although this action has been shown to be independent of the ability to inhibit parietal secretion as measured by hydrogen ion (H+) output, it may be related to stimulation of nonparietal secretion measured here as sodium ion (Na+) output. Five conscious, chair-adapted rhesus monkeys received an infusion of either prostacyclin (PGI2; 125, 175, or 250 ng/kg/min intravenously) or the 15(S), 15-methyl analog of either PGF2α (mePGF2α; 0, 1000, or 2000 ng/kg/min subcutaneously) or PGE2 (mePGE2; 0, 15, or 30 ng/ke/min subcutaneously) on different days. The output of H+, Na+ potassium (K+), and chloride (Cl−) ion were determined using a dye dilution technique during a basal period and following the intragastric administration of an 80-ml water load. PGI2 (175 and 250 ng/kg/min), mePGF2α, and mePGF2 all significantly inhibited H+ output. Both basal and postload Na+ output were increased significantly by mePGE2, while only postload Na+ output was significantly enhanced by mePGF2α. Na+ output was not modified by PGI2. K+ output was unchanged by mePGE2α or mePGF2α; however, postload K+ output was significantly inhibited by the highest dose of PGI2. Both basal and postload Cl− output were suppressed significantly by PGI2 while basal Cl− output was decreased significantly by the higher dose of mePGF2α and postload Cl− output was inhibited by both doses of mePGF2α. In contrast, Cl− secretion was unaffected by mePGE2. Thus, mePGE2 markedly increased nonparietal secretion, while mePGF2α mildly increased and PGI2 did not affect nonparietal secretion. On the basis of these results, a stimulation of nonparietal secretion cannot be considered as the common mechanism for the gastric cytoprotective effect of these prostaglandins.