Changes in catecholamine excretion after short-term tyrosine ingestion in normally fed human subjects

Abstract

The effects of ingesting the aromatic amino acid L-tyrosine on excretion of unconjugated catecholamines (dopamine, norepinephrine, and epinephrine) and tyrosine were studied. (Tyrosine is the circulating precursor for the catecholamines, but only a small fraction of the tyrosine in the body is utilized for catecholamine synthesis.) In 10 of 11 normal volunteer subjects, ingestion of 100 mg/kg tyrosine (in three divided doses, preceding each meal, between 8 AM and 5 PM) for 1 day increased the 24-h excretions of total catecholamines by 25%. Only 0.42% of the tyrosine dose was excreted unchanged, but this was sufficient to increase urinary tyrosine by 138%. Both tyrosine and catecholamine excretions varied diurnally; 60% or more of the total output occurred during the day. Since urinary catecholamines reflect molecules synthesized outside the central nervous system, these findings indicate that tyrosine administration can accelerate catecholamine synthesis in the human sympathoadrenal system, probably by enhancing saturation of tyrosine hydroxylase. Therefore, tyrosine may be useful therapeutically in diseases characterized by peripheral catecholamine deficiencies.

Effect of protein ingestion on urinary dopamine excretion. Evidence for the functional importance of renal decarboxylation of circulating 3,4-dihydroxyphenylalanine in man.

“…The possibility that DOPA might be a constituent ofthe ingested protein or the product ofsynthesis from tyrosine within gut tissues or by intestinal microflora is unlikely since its content in canned tuna is low and the major metabolic fate for DOPA within the gastrointestinal tract is local Renal Dopamine Response to Oral Protein 1691 E E 0 decarboxylation or conjugation. Moreover, if urinary DA responses to protein or tyrosine reported elsewhere are also indicative of systemic release of DOPA prior to renal decarboxylation, the demonstration that oral tyrosine reproduces in rats the protein-related rise in urinary DA and increases plasma levels and urine content of DA in human subjects (10,26,27), implies that the DOPA response to protein is related to the increased availability of tyrosine. This relationship, however, does not depend upon oral administration since tyrosine delivered parenterally also elevates urine and plasma DA (28, 29).…”

Effect of <i>l</i>-<i>p</i>-Tyrosine on the Development of Renal Hypertension in Rats

“…If it occurs, it is possible that the resulting increased pro duction of norepinephrine may act centrally, presumably at the area of the nucleus tractus solitarius [4,6,29], to inhibit sympathetic outflow and/or to inhibit renin release pe ripherally, as is the case for clonidine [31]. Since norepinephrine is also known to exert an inhibitory effect on the enzyme, tyrosine hydroxylase, it may also feed back on this rate-limiting enzyme to inhibit its own syn thesis [9], Acute administration of tyrosine to rats and humans has been shown to increase urinary excretion of epinephrine, norepi nephrine and dopamine [2,3], The results tentatively suggest an increase in peripheral metabolism of those three catecholamines al though the urinary excretion of their metabo lites was not measured. Acute administration of tyrosine to rats also resulted in an accumu lation of mcthoxyhydroxyphenylethylglycol sulfate (MOPEG sulfate), a metabolite of norepinephrine, in brain tissue under these conditions [38,40].…”

“…However, these results have been challenged by others [2]. Alterna tively, Tallman et al [39] have suggested that tyramine may be formed from phenylalanine by decarboxylation to (3-phenylethylamine with subsequent hydroxylation to p-tyrosine.…”

Effects of Tyrosine and Tryptophan Ingestion on Plasma Catecholamine and 3,4-Dihydroxyphenylacetic Acid Concentrations*

“…Other large neutral amino acids (LNAA), such as tryptophan, compete for the limited capacity of the transport systems (1,6,7), so that tyrosine uptake is inversely related to the plasma concentration of competing LNAA (1,8). Increased concentrations of precursor tyrosine can accelerate the synthesis and release of catecholamines within the central nervous system (CNS) (5,9) and peripheral sympathoadrenal tissues (10,11).…”