Sources and physiological significance of plasma dopamine sulfate.
Dopamine in the circulation occurs mainly as dopamine sulfate, the sources and physiological significance of which have been obscure. In this study, plasma concentrations of dopamine sulfate were measured after a meal, after fasting for 4 days, and during i.v. L-DOPA, nitroprusside, or trimethaphan infusion in volunteers; after dopamine infusion in patients with L-aromatic-amino-acid decarboxylase deficiency; in arterial and portal venous plasma of gastrointestinal surgery patients; and in patients with sympathetic neurocirculatory failure. Meal ingestion increased plasma dopamine sulfate by more than 50-fold; however, prolonged fasting decreased plasma dopamine sulfate only slightly. L-DOPA infusion produced much larger increments in dopamine sulfate than in dopamine; the other drugs were without effect. Patients with L-aromatic amino acid decarboxylase deficiency had decreased dopamine sulfate levels, and patients with sympathetic neurocirculatory failure had normal levels. Decarboxylase-deficient patients undergoing dopamine infusion had a dopamine sulfate/dopamine ratio about 25 times less than that at baseline in volunteers. Surgery patients had large arterial-portal venous increments in plasma concentrations of dopamine sulfate, so that mesenteric dopamine sulfate production accounted for most of urinary dopamine sulfate excretion, a finding consistent with the localization of the dopamine sulfoconjugating enzyme to gastrointestinal tissues. The results indicate that plasma dopamine sulfate derives mainly from sulfoconjugation of dopamine synthesized from L-DOPA in the gastrointestinal tract. Both dietary and endogenous determinants affect plasma dopamine sulfate. The findings suggest an enzymatic gut-blood barrier for detoxifying exogenous dopamine and delimiting autocrine/paracrine effects of endogenous dopamine generated in a "third catecholamine system."
Clinical Neuroscience Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892, USA. daveg@box-d.nih.gov
D S
DS
Goldstein
K J
KJ
Swoboda
J M
JM
Miles
S W
SW
Coppack
A
A
Aneman
C
C
Holmes
I
I
Lamensdorf
G
G
Eisenhofer
D000328:Adult; D001142:Aromatic-L-Amino-Acid Decarboxylases / Q000172:deficiency; D001158:Arteries; D001342:Autonomic Nervous System Diseases / Q000097:blood; D015153:Blotting, Western; D004298:Dopamine / Q000031:analogs & derivatives* / Q000097:blood; D015259:Dopamine Agents; D005215:Fasting; D005260:Female; D005502:Food; D005770:Gastrointestinal Neoplasms / Q000097:blood / Q000601:surgery; D006801:Humans; D007980:Levodopa / Q000008:administration & dosage / Q000097:blood; D008297:Male; D009599:Nitroprusside / Q000008:administration & dosage; D011169:Portal Vein; D014294:Trimethaphan / Q000008:administration & dosage
D015259:Dopamine Agents; D009599:Nitroprusside; D007980:Levodopa; C007558:dopamine 3-O-sulfate; D014294:Trimethaphan; D001142:Aromatic-L-Amino-Acid Decarboxylases; D004298:Dopamine