Oral load of tyrosine or L-dopa and plasma levels of free and sulfoconjugated catecholamines in healthy men.

Abstract

The levels of free and sulfoconjugated catecholamines were measured in the plasma of fasting, recumbent normal subjects before and after an oral load of the catecholamine precursors tyrosine or L-dopa. Basal values of sulfoconjugated catecholamines, measured in plasma samples diluted 1:100 were 7998 +/- 540 pg/ml for dopamine sulfate, 2938 +/- 281 pg/ml for norepinephrine sulfate, and 2958 +/- 288 pg/ml for epinephrine sulfate (n = 37 tests in 15 men); these basal values are higher than those reported previously. Neither free nor sulfoconjugated catecholamine concentrations were changed by a tyrosine load (100 mg/kg) that induced a doubling of the plasma tyrosine level or by a meal low in phenylalanine and tyrosine (but otherwise supplying constituents of normal nourishment) that induced a greater than 50% reduction in the plasma tyrosine concentration. After an oral load of L-dopa (125 mg) the following were observed. (1) An extremely large increase (greater than 100-fold) in dopamine sulfate levels was noted, an increase that was less marked in the same subjects given L-dopa (125 mg) plus the peripheral dopa-decarboxylase inhibitor carbidopa (12.5 mg); as expected, free dopamine concentration also was increased. (2) Neither free nor sulfoconjugated norepinephrine concentrations were altered. (3) Epinephrine sulfate but not free epinephrine concentration was increased (more than ten-fold) after L-dopa ingestion alone; this result was unexpected and has to be confirmed before considering its physiological meaning, if any.

Effects of an Intravenous Infusion of Noradrenaline on the Plasma Concentration of Free and Sulfoconjugated Catecholamines in Anesthetized Dogs

“…However, basal values in the dog. reported in the present article, are even greater than those pre viously published [Unger et al, 1980;Cuche et al, 1983;Bovect al.. 1984], As shown in table I, this is in relation with the dilution of plasma samples, as al ready observed in man [Cuche et al, 1985]. This increase related to the dilution of samples, is a still unexplained phenomenon.…”

“…As shown by data (table III. bottom lines), the internal standards were below 100% when free CA were measured, and above 100% when sulfoconjugated CA were mea sured; this phenomenon has been already noted in man [Cuche et al, 1985], but remains unexplained. Since the percentages shown in table III were un changed at any plasma free NA level, this demon strates that the methylation of CA was carried out in Data are expressed as means ± SEM.…”

“…1984;Dunne et al. 1984;Cuche et al, 1983Cuche et al, , 1985, Thus, sulfate conjugation is usually considered as a metabolic pathway for inacti vating CA and making their elimination eas ier. This is likely to be incomplete because the organism has a sulfatase system.…”

Dopaminergic abnormalities in borderline essential hypertensive patients.

“…19 Phenylalanine hydroxylase, which catalyzes phenylalanine conversion to tyrosine, mainly in the liver, has properties similar to those of tyrosine hydroxylase. 20 It is conceivable that oral DOPA administration, increasing DOPA concentration in the portal vein, may suppress phenylalanine hydroxylase and lower plasma tyrosine.…”

Free and Sulfoconjugated Catecholamines in Normotensive Uremic Patients: Effects of Hemodialysis

“…Previous data demonstrate the enhanc ement of Tyr-hydroxylase and monoamine oxidase (MAO) activities with reduction of NE reuptake at nerve terminals in uremic rats [5] and decreased acticity of COMT in erythrocytes of patients with chronic renal failure [34,35], In uremic patients, stimulated release of NE in acute postural testing seems unaffected [14,15,18,36]: moreover, a progressive reduction of the renal excre tion of CA, with increasing degrees of renal insufficiency, has been reported [37], Patients studied here exhibited a manyfold increase of all sulfated CA, as observed in previous studies [19,20], Very recent data regarding plasma sCA in uremia [19] showed higher levels with respect to our findings. These discrepancies may be explained chiefly by an excessive dilution of plasma samples which induces an overestima tion of sCA levels [38,39], The same investigators [19,39] showed 'normal' plasma levels of glucuronoconjugated CA (gCA) in uremic patients. It should be stressed that in normal humans, gCA seem to be barely detectable [23,40]; moreover, total conjugated CA in uremia, measured after mild acid hydrolysis, were shown to be much lower [20] with respect to the above mentioned findings [19],…”