Effects of prostaglandin E2, F2 alpha, and synthetic thromboxane A2 (PGE2, PGF2 alpha, and STA2, respectively) on electrical and mechanical responses of the rabbit cecum were investigated. Transmural electrical stimulation evoked an excitatory junction potential (EJP) and contraction, events that were inhibited by 1 microM atropine or 0.3 microM tetrodotoxin. Indomethacin (up to 30 microM) modified neither the membrane potential nor the muscle tone but did inhibit amplitudes of the EJP and the twitch contraction. In the presence of 30 microM indomethacin, PGE2 (below 1 nM) had no effect on the membrane potential or muscle tone, while PGE2 (above 10 nM) contracted the cecal tissues, without depolarization. PGE2 enhanced the twitch contraction and restored the EJP in the presence of 30 microM indomethacin. Acetylcholine (0.1-3 microM) depolarized the membrane, but in the presence of 30 microM indomethacin, this depolarization was inhibited. PGE2 (0.1-100 nM) prevented these inhibitory actions of indomethacin. PGF2 alpha (0.1-100 nM) had weaker actions than PGE2 while STA2 (0.1-100 nM) had no effect on muscarinic responses. Thus muscarinic responses are augmented by primary prostaglandins.