1989 Volume 25 Issue 4 Pages 125-135
Fujii, K., Okajima, M., Kawahori, K., Murakami, Y. and Shimatani, T. Effect of α2-adrenergic receptor antagonist (Midaglizole) on gastrointestinal motility in conscious dogs. Jpn. J. Smooth Muscle Res., 1989, 25 (4), 000-000, 1989 To clarify the physiological role of the mechanism that adrenergic nerve inhibits Ach release from intramural cholinergic nerve endings, the influence of Midaglizole, α2-adrenergic receptor antagonist, to postpran-dial gastrointestinal motilities in conscious dogs was investigated.
Postprandial motilities of gastric antrum, duodenum, ileum, and colon were significantly enhanced by Midaglizole (3.0-5.0 mg/kg body weight, i.v, ). These excitatory responses were abolished by atropine (0.05-0.1 mg/kg body weight, i.v.). On the other hand, in most cases (29 cases out of 32), when Midaglizole was administered during quiesent phase of IMC, no change occurred in gastrointestinal motility. However, after subliminal dose of pentagastrin or cisapride, which stimulated Ach release from intramural cholinergic neuron without development of motility, was administered, Midaglizole induced phasic, postpran-dial motility-like contraction in gastrointestinal tract. Even in the fasted state, when Midaglizole was administered intragastrically, irregular contractions with high amplitude occurred in every regions from gastric antrum to colon. And these excitatory responses were abolished by atropine. Similar reaction was observed also in truncal vagotomized dogs.
These results suggest that it is the physiological mechanism that adrenergic nerve presynaptically inhibits Ach release from intramural cholinergic neuron, which is the main mechanism of development of postprandial motility, acting on α2-adrenergic receptor, and has tonic control of postprandial motility.
