The effects of exogenously applied prostaglandins on the contractile responses of the gallbladder and sphincter of Oddi isolated from guinea pigs were examined in normal and indomethacin-treated preparations. Indomethacin reduced the tone and the contractile responses to transmural stimulation and to exogenously applied ACh of the gallbladder, while the tone and contractile responses of the sphincter of Oddi were little affected by indomethacin. Prostaglandins E₁, E₂ and F_2α potentiated the contractile responses of the gallbladder to transmural stimulation and ACh, and furthermore, treatment with indomethacin enhanced the potentiating effects of prostaglandins E₁ and E₂ but not the effect of PGF_2α. The reduced tone and contractility of the gallbladder were restored to the control level by addition of PGE₁ and PGE₂ but not by PGF_2α. These results suggest that endogenous PGE₁ and PGE₂ may play an important role in neurogenic control of contractility of the gallbladder, but not of the sphincter of Oddi.

In studies on prostaglandin (PG) synthetase activity in the guinea pig gallbladder, prostaglandin E₂ and F_2α (PGE₂ and PGF_2α) were enzymatically formed from arachidonic acid using the 105,000-g precipitate fraction. The amount of PGE₂ synthesized was about four times larger than PGF_2α. Indomethacin (1–3 µM) inhibited both the PG synthesis and the contractile response to transmural stimulation in the gallbladder. These findings suggest that the inhibitory effect of indomethacin on the contractility of the gallbladder is related to the inhibition of PG synthesis, and that endogenous PGE₂ is involved in the contractility of this tissue.

Abstract-Effects of C-terminal octapeptide of cholecystokinin (CB-CCK) and prostaglandins E1, E2 and F2ai on noradrenaline-induced responses and 3H -noradrenaline release in the gallbladder and sphincter of Oddi of guinea pigs were examined. In the sphincter of Oddi, noradrenaline in low concentrations induced a relaxation which was blocked by either phen tolamine or propranolol, while noradrenaline in high concentrations induced a contraction which was blocked by phentolamine. These results suggest the existence of excitatory and inhibitory a-receptors and inhibitory 8 receptors in the sphincter of Oddi. In the gallbladder, the adrenergic receptors are a-excitatory and (3-inhibitory. CB-CCK (10-9 g/ml) poten tiated both contractile and relaxing responses to noradrenaline, in the gallbladder. The same concentration of prostaglandins potentiated only contractile response to noradrenaline. In the sphincter of Oddi, nor adrenaline-induced responses were not affected by CB-CCK and prosta glandins. Prostaglandins inhibited 3H-efflux evoked by electrical stimu lation, while CB-CCK had no effect on the 3H-efflux from both preparations. These results suggest that CB-CCK enhances the contractile and relaxing responses to noradrenaline, and that prostaglandins act in a similar way on the postsynaptic response and, in addition, inhibit presynaptically the release of noradrenaline in the gallbladder. In the sphincter of Oddi, only prostaglandins inhibit the presynaptic event.

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