Abstract
Exposure of the rat to restraint and water immersion stress enhanced a characteristic gastric movement in a 2 to 4-hr latent period. The mechanism of producing such gastric movement was studied in connection with changes in the sympatho-adrenal activity. Acute bilateral adrenalectomy and reserpine pretreatment significantly hastened occurrence of the gastric movement and guanethidine pretreatment showed a similar tendency. Epinephrine content in the adrenals of the stressed group markedly decreased at the time of occurrence of the gastric movement. Urinary excretion of epinephrine and norepinephrine continued to increase for 3 hr and for 6 hr respectively, after the onset of stress, and both excretory rates declined thereafter. Epinephrine and norepinephrine were much more effective on depressing the stressinduced gastric movement than cortisone and ACTH. It was suggested that: 1) at the initial stage of stress, the adrenal function as well as the sympathetic nervous function was activated, and a large amount of epinephrine and norepinephrine was secreted, which brought about an inhibition of the gastric movement; 2) at the subsequent stage, the parasympathetic nervous function became more prominent than the sympathoadrenal one and initiated the gastric movement; and 3) contribution of corticosteroids and/or ACTH to the gastric movement was small, if any.