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Cardiovascular effects have been attributed to the amino acids which are precursors of catecholamines or other neurotransmitters. To study if even other amino acids may exert cardiovascular or ventilatory effects, a number of various acidic, basic and neutral L-amino acids were injected intravenously to anaesthetised normotensive rats at the doses of 0.2-1.6 mmol/kg. All amino acids were able to produce either blood pressure, heart rate or ventilation rate changes. Hence, in this study the production of cardiovascular or ventilatory effects was not limited to the known precursors of neurotransmitters. Therefore, in addition to increased formation and release of neurotransmitters, other mechanisms are apparently involved in the cardiovascular and ventilatory effects of various L-amino acids.

Tyrosine exerts potent cardiovascular effects: smaller doses induce tachycardia and hypertension while higher doses induce bradycardia and hypotension. However, the direct cardiac effects of this amino acid have not been characterised. In the present study increasing doses of L-tyrosine were administered to the perfusate of isolated rat (0.01-10.0 mg) and rabbit (0.5-40.0 mg) hearts. Heart rate and isometric force of contraction or amplitude of contractions, and either perfusion pressure or flow of perfusate were recorded. In rat hearts L-tyrosine decreased heart rate and isometric force of contraction. In rabbit hearts L-tyrosine also decreased heart rate and amplitude of contractions. The effects on coronary vasculature were variable. In rat hearts, high doses of L-tyrosine induced bi-phasic changes with initial coronary dilatation, followed by vasoconstriction. In rabbit hearts the predominant effect of L-tyrosine was coronary artery constriction. These results show that the inhibitory cardiovascular effects of L-tyrosine in vivo may be at least in part, explained by direct cardiac effects of this amino acid.

There are conflicting reports on the blood pressure effects of tyrosine. The aim of this study was to establish complete dose-response relationships and to compare the effects of various modes of administration of L-tyrosine in anaesthetised normotensive and spontaneously hypertensive rats. The intravenous injection of L-tyrosine, 0.2–0.4 mmol/kg, produced tachycardic and hypertensive effects in both species. The higher doses (0.8–1.6 mmol/kg) produced marked bradycardiac and hypotensive responses. Intracerebroventricular administration of L-tyrosine, 0.005–0.1 mmol/kg, had no statistically significant effects. Chronic dietary administration of L-tyrosine, approximate daily doses of 0.7–55 mmol/kg was also without any significant effects. These results suggest that the controversies in the earlier studies could be due mainly to differences in doses and modes of administration. Our results also suggest that the cardiovascular effects of tyrosine are peripheral rather than central in origin although a central site of action cannot be excluded.

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.

Tyrosine is the precursor of catecholamines. Small doses of tyrosine produce tachycardia and hypertension while higher doses produce bradycardia and hypotension in anaesthetised rats. The mechanism of these effects has not been established. An increased synthesis and release of catecholamines has been suggested to be the mechanism. Various pretreatments were given to anaesthetised Wistar rats to study the influence of a blockade of L-tyrosine metabolism and thus a blockade of catecholamine synthesis, on these cardiovascular effects: valine, which inhibits tyrosine uptake into brain, alpha-methyl-p-tyrosine, which blocks the rate-limiting enzyme, tyrosine hydroxylase, carbidopa and benserazide, which both inhibit dopa decarboxylase, and desipramine, which blocks catecholamine re-uptake. Benserazide and alpha-methyl-p-tyrosine partially blocked the stimulatory effects of tyrosine. None of the pretreatments were able to block effectively the inhibitory effects of L-tyrosine. Therefore, the metabolism of tyrosine to form catecholamines may be involved in the stimulatory but not in the inhibitory cardiovascular effects of L-tyrosine. Valine pretreatment did not antagonize the depressant effects of tyrosine. Since valine blocks the uptake of L-tyrosine into the brain, the depressant effects of L-tyrosine might be peripheral rather than central in origin.