Abstract

AbstractTransmural stimulation applied to the isolated sphincter of Oddi from rabbit caused a transient contraction. On termination of stimulation, a rapid second contraction was superimposed, then followed by a relaxation and inhibition of auto-maticity. Atropine inhibited the initial component during stimulation. The late second component was, however, little affected by atropine. On the other hand, the contractile response to exogenously applied acetylcholine was antagonized by atropine. All responses to transmural stimulation were completely abolished by tetrodotoxin 1.55 × 10-7 M. Both initial and late components of contractile response to transmural stimulation were significantly reduced in cold stored preparations depending on the period of storage, and under N2 gas-bubbling anoxia. The contractile response to exogenous acetylcholine, however, was not reduced under such conditions. Both initial and late components were unaffected by a ganglionic blocking agent and adrenergic alpha and beta blocking agents, alone or combined. Both components were significantly inhibited by pretreatment with hemicholinium-3, or noradrenaline, however, the response to exogenous acetylcholine was little affected by pretreatment with noradrenaline. The physostigmine-potentiated late component was reduced by atropine, whereas the late component was not potentiated by physo-stigmine in the presence of atropine. It is clear that the initial component is mediated through the release of acetylcholine from the intramural postganglionic cholinergic neurones. These results indicate that the late component may also be related to acetylcholine released from the same neurones.

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