Abstract
Summary
Administration of methyldopa (L-a-methyldopa) to reserpine-treated dogs and rabbits results in restoration of pressor responses to tyramine. The amine metabolites of methyldopa, α-methyldopamine and α-methylnorepinephrine, cause similar but more prompt enhancement of tyramine responses with the latter compound showing maximum potency and more prompt onset of effect. That the effects of methyldopa are due to its amine metabolites is also indicated by the fact that D-α-methyldopa, which is not decarboxylated, is inactive. Present evidence favors α-methylnorepinephrine as the mediator responsible for the blood pressure lowering produced by methyldopa in man, as well as the preservation and restoration of tyramine responses following administration of the parent drug.
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