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Exposure of rats to restraint plus water-immersion (25 degrees C) stress produces a marked increase in gastric motility with hypothermia. Although this phenomenon was generally considered to be due to centrally mediated cholinergic mechanisms, the present study was designed to elucidate some local peripheral mechanism in enhancing gastric motility with hypothermia. After the onset of water-immersion (37-17 degrees C), body temperature rapidly varied depending on water temperature and gastric motility changed in its pattern with stress duration; increase in gastric motility reached a maximum at 25 degrees C but declined at 17 degrees C. These alterations of gastric motility pattern were not primarily associated with activation or decline of the sympatho-adrenal system. In these stressed rats, either vagally intact or vagotomized, contractile responses of the stomach to i.v. or i.a. administration of bethanechol and acetylcholine, but not to that of histamine, were markedly augmented by lowering body temperature. Similar observations were noted in rats exposed to restraint plus cold (6 degrees C) stress. These results emphasize the possibility that augmentation of gastric motility during water-immersion (25 degrees C) occurs at least in part through local peripheral mechanisms of increasing the contractile sensitivity of the stomach to acetylcholine with hypothermia.

Stress procedures lowering body temperature augment gastric motility by increasing the sensitivity to acetylcholine in rats.