Pre- and postjunctional effects of prostaglandin E2, prostaglandin synthetase inhibitors and atropine on cholinergic neurotransmission in guinea pig ileum and bovine iris

Abstract

The effects of prostaglandin [PG]E2, arachidonic acid, PG synthetase inhibitors and atropine on cholinergic neuromuscular transmission were examined in isolated guinea pig ileum longitudinal muscle and bovine iris sphincter muscle. PGE2 and arachidonic acid enhanced contraction responses induced by nerve stimulation. PGE2 enhanced contraction responses to acetylcholine and direct muscle stimulation, approximately to the same extent as those to nerve stimulation. PG synthetase inhibitors (indomethacin, meclofenamic acid and eicosatetraynoic acid) reduced contraction responses to nerve stimulation or acetylcholine, and annulled the stimulant effect of arachidonic acid. Basal and nerve-induced efflux of acetylcholine from the eserinized tissues, as measured by mass fragmentography, was unaltered by PGE2, but diminished slowly during indomethacin. Subsequent PG administration increased nerve-induced release of acetylcholine. Atropine markedly increased overflow of acetylcholine form stimulated preparations of both types. Muscarinic receptors, causing diminished acetylcholine release in eserinized tissue, may be present at postganglionic terminals. During atropine, an effect of PGE2 on acetylcholine release could still not be seen. Using physicochemical determination of acetylcholine, earlier reports, using bioassay, claiming enhanced release of transmitter during PGE2 treatment were not verified. PGE2 may regulate contractility and tone of the smooth muscle cells.