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On the β-hydroxylation of (±)-α-methyldopamine in vivo

1968; Elsevier BV; Volume: 5; Issue: 1 Linguagem: Inglês

10.1016/0014-2999(68)90160-x

1879-0712

Arvid Carlsson, Jean-Jacques Meisch, Bertil Waldeck,

Pharmacological Receptor Mechanisms and Effects

Tritium-labelled (±)-a-methyldopamine was given i.v. to mice. The amine was taken up by the heart and converted to 3H-a-methylnoradrenaline. The hydroxylation product seemed to have the erythro configuration. It is suggested that only (+)-a-methyldopamine is β-hydroxylated. The effects of protriptyline, reserpine, sodium diethyldithiocarbamate (DDC) and bis(4-methyl-l-piperazinylthiocarbonyl)disulphide (EWP 815), which inhibit the amine-transport mechanism of the cell membrane of the adrenergic neuron, the granular amine-storage mechanism and the enzyme dopamine β-hydroxylase, respectively, were investigated. In contrast to earlier in vitro observations blockade of the granular storage-mechanism by reserpine caused no corresponding decrease in dopamine β-hydroxylase activity in vitro. Nialamide caused release of 3H-a-methyldopamine, probably by an indirect action, caused by accumulation of endogenous monoamines. Inhibition of catechol-O-methyl transferase by a-propyldopacetamide (H 22/54) caused a twofold increase in the levels of both a-methylated catecholamines in the heart.