Exogenous tyrosine lowers blood pressure in spontaneously hypertensive rats (SHR). The artificial sweetener aspartame also elevates blood and brain tyrosine levels in rats by being hydrolyzed to phenylalanine, which is then rapidly hydroxylated to tyrosine in the liver. Hence we tested the ability of aspartame; its hydrolytic products phenylalanine, aspartic acid and methanol; and of tyrosine itself to lower blood pressure in SHR. For one week prior to experimentation rats were acclimated to the indirect blood pressure measurement technique; on the day of an experiment they received I.P. injections (mg/kg) of aspartame (12.5-200), tyrosine (25-200) or phenylalanine (100-200), or of aspartic acid or methanol in the doses theoretically contained within 200 mg/kg aspartame. Animals receiving 50, 100 or 200 mg/kg of aspartame exhibited maximum falls in blood pressure of 17.3, 24.2 and 19.3 mmHg, respectively. All changes were significant, as determined by ANOVA and the Newman-Keuls test (p less than 0.05). Tyrosine or phenylalanine also lowered blood pressure, but aspartic acid or methanol produced no significant effects. Co-administration of aspartame with valine, a large neutral amino acid that competes with phenylalanine or tyrosine for brain uptake, attenuated aspartame's hypotensive effect. These observations suggest that the neurochemical changes produced by aspartame lead to predicted tyrosine-induced changes in blood pressure.
Previous studies have demonstrated the ability of tyrosine (TYR), the amino acid precursor of catecholamines, to increase blood pressure in rats made hypotensive by haemorrhage. Other studies have shown that supplementation of the diet with TYR can reverse certain neurochemical and behavioural consequences associated with acute stress. Such studies demonstrate that during conditions of enhanced neuronal firing catecholamine synthesis is accelerated when additional precursor TYR is made available. In these situations the rate-limiting enzyme of catecholamine synthesis, tyrosine hydroxylase, activated via phosphorylation, becomes responsive to additional TYR. Our experiments were designed to study the ability of dietary TYR (3.7%, or 4X the normal amount), to prevent the rapid fall in blood pressure observed during acute haemorrhage. Rats consuming the high TYR diet (5 days) maintained arterial blood pressure (systolic, diastolic and mean) at significantly greater values during the period of acute haemorrhagic insult than animals maintained on a control diet. Rats fed the high TYR diet had significantly greater levels of the amino acid in the heart, adrenal glands, liver, kidney, brainstem, spleen and semimembranosus pars caudalis muscle. We conclude that TYR can be stored and most likely utilized in the synthesis of catecholamines for the maintenance of arterial blood pressure during acute haemorrhage. These results are of particular importance in light of the fact that most total parenteral nutrition solutions contain very little if any TYR.
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