Modulation on neuromuscular transmission by endogenous and exogenous prostaglandins in the guinea-pig mesenteric artery.

1. At concentrations of 2.8 x 10(-8)-2.8 x 10(-6) M, prostaglandins (PGs; PGE(1), PGE(2) and PGF(2alpha)) had no effect on membrane potential and resistance of smooth muscles of the guinea-pig mesenteric artery. PGs (2.8 x 10(-8) M) suppressed the contraction evoked by perivascular nerve stimulation, but did not suppress the contraction evoked by direct muscle stimulation.2. PGs (2.8 x 10(-8) M) suppressed the e.j.p.s evoked by repetitive perivascular nerve stimulation but preserved the facilitation process of e.j.p.s evoked by any given stimulus frequency (0.1-1.0 Hz).3. The relationships between e.j.p. amplitudes and Ca plotted on log scales in the presence or absence of PGE(2) were not parallel. High concentrations of Ca prevented the inhibitory actions of PGs on the amplitude of e.j.p.s.4. PGE(2) did not suppress the activity of nerve fibres contributing to the generation of e.j.p.5. Indomethacin (10(-6) M) enhanced the amplitude of e.j.p.s and the frequency of miniature e.j.p.s with no change in the membrane potential and resistance of smooth muscles; these actions of indomethacin were suppressed by PGE(2) (2.8 x 10(-8) M).6. Phentolamine (10(-7) M) enlarged and yohimbine (10(-7) M) reduced the amplitude of the first e.j.p. evoked by a train stimulation, but the maximum amplitude of e.j.p., after the facilitation was completed, was in both cases much larger than that observed in the control. The enhancement of the transmission process was also suppressed by PGs (2.8 x 10(-8) M).7. The results indicate that in the guinea-pig mesenteric artery, PGs mainly suppress chemical transmitter release from nerve terminals due to interactions with Ca influx, but not due to interaction with presynaptic alpha-adrenoceptors. Endogenous PG may act as a regulator substance in neuromuscular transmission.