Gastric hypersecretion by intracisternal TRH: dissociation from hypophysiotropic activity and role of central catecholamine.

Intracisternal injection of the TRH analogs, MK 771 (0.01-1 micrograms) or A 3475 [pGlu-His-(1,3'-dicarboxymethyl)-Pro-NH2] (0.1-1 micrograms), dose-dependently stimulated gastric acid secretion in pylorus-ligated rats although A 43475 was devoid of TSH-releasing activity by cultured anterior pituitary cells. Depletion of brain catecholamine by combined administration of the neurotoxic agent, 6-hydroxydopamine, and the catecholamine synthesis inhibitor, alpha-methyl-ptyrosine, completely abolished intracisternal TRH-induced stimulation of gastric secretion. Blockade of dopamine receptors by intracisternal haloperidol, peripheral depletion of catecholamine by chronic treatment with guanethidine combined with acute adrenalectomy or cervical cord transection at C5 level, did not modify gastric response to TRH. These results suggested that the stimulation of gastric secretion by intracisternal TRH is unrelated to its hypophysiotropic activity and required the integrity of central but not peripheral catecholaminergic system.