ArticleTimimi KS, Bedwani JR, Stanton TW.
Br J Pharmacol. 1978 May;63(1):167-76.
1 Investigations were made into the effects of prostaglandin E(2) (PGE(2)) and a prostaglandin endoperoxide analogue (Upjohn compound U-46619) on the responses of the rat anococcygeus muscle to field stimulation of the intrinsic sympathetic nerves, and to exogenous noradrenaline. The effects of PGE(2) on responses to stimulation of intrinsic inhibitory nerves were also studied.2 PGE(2) (5.6 x 10(-8) or 2.8 x 10(-6) mol/l) decreased motor (sympathetic) responses to field stimulation at all frequencies tested (2 to 24 Hz). The prostaglandin also reduced the inhibitory responses to field stimulation, seen when the tone of the preparation had been raised and its sympathetic innervation had been blocked by guanethidine. However, these inhibitory responses were also reduced by other spasmogens (carbachol and 5-hydroxytryptamine) which, like PGE(2), further increased the tone of guanethidine-treated preparations.3 At a concentration of 5.6 x 10(-8) mol/l, PGE(2) had no effect on responses to noradrenaline, whereas at a fifty-fold higher concentration the prostaglandin potentiated these.4 Unlike PGE(2), U-46619 (5.6 x 10(-8) mol/l) greatly potentiated motor responses to field stimulation, at frequencies from 0.75 to 24 Hz. This effect did not represent a specific facilitation of sympathetic neurotransmission, as responses to carbachol and 5-hydroxytryptamine, as well as to noradrenaline, were also potentiated.5 The results are discussed in relation to the effects of prostaglandins and prostaglandin endoperoxides on neuroeffector transmission in other sympathetically innervated tissues. It is concluded that PGE(2) inhibits sympathetic neurotransmission in the rat anococcygenus muscle by a prejunctional action, whereas the predominant effect of U-46619 is direct excitation of the muscle. The effect of PGE(2) on inhibitory responses to field stimulation may represent an interference with inhibitory neuroeffector transmission in this tissue, or may simply be a consequence of the spasmogenic action of the prostaglandin.