Effect of alpha-methyldopa on alpha-noradrenergic receptor binding sites in the mouse brain.
alpha-Methyldopa (alpha-MD) was administered intraperitoneally into adult male mice and its effect on alpha 1- and alpha 2-noradrenergic receptor binding sites in the brain was investigated, using [3H]WB-4101 and [3H]clonidine, respectively. A single injection of 50-200 mg/kg alpha-MD abolished the high affinity binding to alpha 2-receptor sites and only the low affinity binding was observed with lower Bmax values. A significant effect of alpha-MD on alpha 1-receptor sites was not detected even after repeated injections (200 mg/kg/day X 3). Pretreatment with fusaric acid or diethyldithiocarbamate (inhibitors of dopamine-beta-hydroxylase) exerted no influence on the actions of alpha-MD on alpha 2-receptor sites, whereas NSD-1055 (an inhibitor of dopa decarboxylase) inhibited the effects of alpha-MD. It is concluded, therefore, that alpha-methyldopamine, a decarboxylated metabolite of alpha-MD, may be responsible for the reducing effect of alpha-MD on alpha 2-receptor sites.[1]References
- Effect of alpha-methyldopa on alpha-noradrenergic receptor binding sites in the mouse brain. Oide, M. Pharmacology (1984) [Pubmed]
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