Intracisternal or intracerebroventricular injection of TRH (0.1-10 micrograms) in rats stimulated the secretion of gastric acid and pepsin secretion, increased gastric mucosal blood flow and gastric contractility and emptying, induced gastric hemorrhagic lesions and aggravated experimental ulcers elicited by aspirin, serotonin or indomethacin. TRH action was dose-dependent, rapid in onset and central nervous system-mediated by activation of the parasympathetic outflow to the stomach and cholinergic receptors. The stable TRH analog, RX 77368, was more potent and longer lasting than TRH. TRH and its stable analog appear as new chemical probes to produce centrally-mediated vagal-dependent stimulation of gastric function and experimental ulcers. The physiologic role of endogenous TRH in the central regulation of gastric function and ulceration remains to be established.
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