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Abstract
Recently it was shown that the rate-limiting step in noradrenaline (NA) biosynthesis is the hydroxylation of tyrosine to DOPA (1, 2). The enzyme which catalyzes this conversion, tyrosine hydroxylase, has been isolated from various tissues and studied extensively (3, 4, 5). Several tyrosine analogues and catechols were shown to inhibit tyrosine hydroxylase, and α-methyl-tyrosine (α-MT) can be considered as one of the most potent inhibitors (4, 6). α-MT lowers endogenous levels of NA and the mechanism of this depletion has been ascribed to a blockade of the enzymatic synthesis of NA at the tyrosine hydroxylase step (7). The present study shows that after giving α-MT the same α-methylated catecholamines are formed in vivo as after treatment with α-methyl-DOPA, but the concentration in heart and brain are lower.
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