Inhibitory Effect of Prostaglandins on Isosmotic Fluid Transport by Rabbit Gall‐Bladder In Vitro, and its Modification by Blockade of Endogenous PGE‐Biosynthesis with Indomethacin

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Abstract
In the presence of indomethacin serosal application of PGEi and PGE2 caused significant inhibition of net isosmotic fluid transport by the gall‐bladder with maximum effect (50%inhibition) at 0.5ftgPGE/ml. Mucosal application was much less effective. PGF2a was about 100 times less potent than PGE. In the absence of indomethacin the sensitivity to low concentrations of PGEi was about 10 times less than in the presence of this drug (p < 0.001). Maximum effective doses of PGEi depressed the unidirectional Na+‐efflux about 35%and the Na+‐influx about 20%.Transepithelial potential difference and ohmic resistance remained unchanged. It is concluded that PGE inhibits isosmotic fluid transport by an effect mainly on the active component of the transfer process. In the absence of indomethacin endogenous PGE2 (but not PGEi) was released to both serosal and mucosal medium. Net release to mucosal medium was 35–600 pg.h‐1.mg dry weight‐1; release was higher to the serosal medium. Mucosal concentrations of 0.2–4.5 ng PGEa/ml were independent of the serosal concentration, which did not exceed 0.8 ng/ml under the present conditions. The data suggest that mucosal PGEs‐release originates, in part at least, from the epithelial cells. Indomethacin (10 μg/ml) blocked almost completely thein vitroPGE‐biosynthesis.