Effects of exogenous and endogenous prostaglandins on the fast phase of contraction of the guinea-pig vas deferens produced by electrical field stimulation.

The initial, fast phase of contraction of the guinea-pig vas deferens produced by electrical field stimulation (10 pulses) was dose-dependently and completely inhibited by prostaglandin (PG) E2, sulprostone and, at high concentrations, by cicaprost. Sulprostone was more potent than PGE2 indicating that the EP3 receptor was involved. Cicaprost (a PGI2 analogue) apparently had weak EP3 receptor against activity. At low concentrations, cicaprost potentiated the contractions of the vas deferens, presumably by acting on an IP receptor. Exogenous arachidonic acid also dose-dependently and completely inhibited contractions of the guinea-pig vas deferens. The action of arachidonic acid was delayed when compared to PGE2 and was inhibited by indomethacin, suggesting that the arachidonic acid was converted to PGE2 by the vas deferens. Indomethacin (1.4 to 6.0 microM) had no significant, potentiating effect on the contractions of the guinea-pig vas deferens which suggests that endogenous PGs do not normally inhibit this fast phase of contraction. In higher concentrations, the contractions were reduced by indomethacin. The fast phase of concentration of the guinea-pig vas deferens consisted of 3 components. PGE2, sulprostone and arachidonic acid inhibited all components. The order of inhibition of the components was component 2, then component 3, followed by component 1.