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Pharmacology of Adrenergic, Cholinergic, and Drugs Acting on Other Receptors in Gastrointestinal Muscle

1982; Springer Science+Business Media; Linguagem: Inglês

10.1007/978-3-642-68474-6_9

1865-0325

E. E. Daniel,

Ion channel regulation and function

The smooth muscle of the gastrointestinal (GI) tract is universally capable of myogenic electrical and mechanical activity (Daniel et al. 1960; Daniel and Sarna 1978). In a few instances, e.g., esophageal smooth muscle in some species (Christensen and Daniel 1966, 1968; Chan and Diamant 1976; Sarna et al. 1977) and guinea-pig small intestine (see Bolton 1979), its oscillations are not spontaneous but can be initiated by acetylcholine acting on muscarinic receptors in smooth muscle. Sphincteric regions which exert continuous tension may spike continuously, unrelated to myogenic oscillatory activity or acetylcholine release (Asoh and Goyal 1975). Elsewhere, atropine or other antagonists at muscarinic receptors or tetrodotoxin acting to prevent Na-dependent action potentials of nerves do not affect this myogenic activity. Myogenic activity in most regions consists of periodic membrane oscillations, called slow waves, electrical control activity (ECA) or pacemaker activity, on which are superimposed spikes or action potentials. Slow waves or ECA without spikes are not accompanied by contractile activity. Contractions are usually but not always accompanied by spikes; there may be massive depolarisation leading to inactivation of spike mechanisms or contraction from release of Ca2+ stores. In vitro, canine stomach circular muscle from some regions responds to acetylcholine by an increase in amplitude and duration of the plateau phase of the myogenic oscillation exclusive of any spikes; these effects are accompanied by contractions (Daniel 1965; Szurszweski 1975; El-Sharkawy et al. 1978; Morgan et al. 1978; El-Sharkawy and Szurszewski 1978).