Influence of the H2-receptor blocking agent metiamide on the clonidine-induced changes in the brain catecholamine turnover.

Metiamide (800 micrograms intracerebroventricularly to rats) enhanced the DOPA accumulation in noradrenaline-predominant brain areas following DOPA decarboxylase inhibition and it accelerated the alpha-methyltyrosine-induced disappearance of noradrenaline in the brain, both normally and after clonidine (0.1 mg/kg i.p.). These findings indicate that metiamide stimulates the release of noradrenaline. They can explain why metiamide antagonizes the clonidine-induced hypotension.