Further studies on the mechanism of the cardiovascular effects of L-tyrosine.

Tyrosine is the precursor amino acid of catecholamines. Low doses of tyrosine produce tachycardia and hypertension, while higher doses induce bradycardia and hypotension in anaesthetised rats. The mechanism and site of action of L-tyrosine are not fully understood. Eight groups of Wistar rats received different pretreatments in order to study the influence of blockade of various receptor mechanisms on the cardiovascular effects of L-tyrosine. The effects mediated by the autonomic nervous system were inhibited by ganglion blockade (hexamethonium), by alpha 1- and beta 1-adrenoceptor blockade (prazosin and atenolol) and by parasympathetic acetylcholine receptor blockade (atropine). The possible role of histamine receptors was studied by inducing H1 and H2-receptor blockade (diphenhydramine and cimetidine, respectively). The effect of inhibition of prostaglandin synthesis by indomethacin was also studied. The L-tyrosine-induced tachycardia was completely blocked by atenolol. Both atenolol and prazosin partly inhibited the hypertensive effects of low doses of tyrosine. The tyrosine-induced bradycardia was not inhibited, and the hypotension was only partly blocked by the pretreatments. Therefore, adrenergic mechanisms seem to mediate the stimulatory cardiovascular effects of tyrosine. The depressant effects of high doses of tyrosine do not appear to be mediated by cholinergic activation, histamine receptor activation, or prostaglandin synthesis.