STUDIES ON THE EXPERIMENTAL GASTROINTESTINAL ULCERS PRODUCED BY RESERPINE AND STRESS : II. ULCEROGENIC ACTIVITIES OF RESERPINE AND ITS ANALOGUES

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The mechanism of ulcer formation by reserpine has been studied by many investigators. Recently, it was demonstrated that even a small dose of reserpine could produce considerably severe ulcers when combined with stress such as restraint (1), conflict (2), electrical stimulation of the hypothalamus (3, 4) and electrical shock through a grid in the floor (4). Concerning the site of action of reserpine, Blackman <I>et al</I>. (5) have described that reserpine-like drugs cause gastric hemorrhage by a mechanism which has an important central component and which involves the liberation of serotonin. On the other hand, Nicoloff <I>et al</I>. (6) reported that norepinephrine administered into the gastric artery provoked ulceration when active acid secretion was present. From these findings it may be considered that ulcers could be produced by peripheral as well as central mechanisms. The author (7) has previously shown that a decrease in serotonin contained in the enterochromaffin cell and norepinephrine contained in vasoconstrictive nerve endings caused by reserpine and stress had close correlation with ulcer formation. In the present paper differences in the ulcerogenic activities between reserpine and its analogues combined with electrical shock through a grid on the floor were investigated. Reserpine analogues used in this study involved two types of drugs, those that release peripheral monoamines and those that release central monoamines.
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STUDIES ON THE EXPERIMENTAL GASTROINTESTINAL ULCERS PRODUCED BY RESERPINE AND STRESS : II. ULCEROGENIC ACTIVITIES OF RESERPINE AND ITS ANALOGUES

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