The effects of prostaglandin E2 (0.2 μM) and indomethacin (50 μM) on the rebound of smooth muscle cells of the guinea-pig taenia coli were studied. Stimulation of the non-cholinergic, non-adrenergic, intramural nerves caused membrane hyperpolarizaiton, known as the inhibitory junction potential (I.J.P.). This hyperpolarization was followed by a rebound depolarization and a rather small rebound contraction in quiescent preparations; the rebound depolarization was often accompanied by action potentials, resulting in a pronounced rebound contration. The effects of prostaglandin E2 (PGE2) on the membrane were comparable with the phenomena observed during the rebound, i.e. membrane depolarization, development of action potentials and contraction of the smooth muscle cells. Furthermore, an increase in amplitude of the I.J.P., enhancement of the spike discharge and a concomitant increase in rebound contraction were observed in the presence of PGE2. Indomethacin did not modify the membrane potential or the amplitude of the I.J.P., but inhibited the rebound contraction and suppressed the development of action potentials during the rebound. The action of PGE2 on the smooth muscle cell membrane was not modified by indomethacin, but the rebound contraction in the presence of both compounds was decreased. These experimental results indicate: that the rebound contraction is accompanied by depolarization of the membrane following the hyperpolarization caused by stimulation of the non-cholinergic non-adrenergic nerves; that the rebound activity can be mimicked by PGE2; that indomethacin does not interfere with the action of PGE2 applied exogenously and that the observations are consistent with the assumption that prostaglandins might be involved in the rebound. © 1979.
