This Article Full Text Full Text (PDF) Submit a related Letter to the Editor Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Copyright Permission Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Goldstein, D. S. Articles by Eisenhofer, G. Search for Related Content PubMed PubMed Citation Articles by Goldstein, D. S. Articles by Eisenhofer, G.

Sources and Physiological Significance of Plasma Dopamine Sulfate

Clinical Neuroscience Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892; Children’s Hospital Division of Genetics, Harvard Medical School, Boston, Massachusetts 02115; The Diabetes and Nutrition Research Laboratory, St. Luke’s Hospital, Kansas City, Missouri 64111; UCL Medical School, Whittington Hospital, London NI9 3UA, United Kingdom; University of Göteborg, Göteborg S-41390, Sweden

Address all correspondence and requests for reprints to: Dr. David S. Goldstein, Building 10, Room 6N252, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892. E-mail: daveg{at}box-d.nih.gov

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 iv 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."

This article has been cited by other articles:

				W. H. A. de Jong, G. Eisenhofer, W. J. Post, F. A. J. Muskiet, E. G. E. de Vries, and I. P. Kema Dietary Influences on Plasma and Urinary Metanephrines: Implications for Diagnosis of Catecholamine-Producing Tumors J. Clin. Endocrinol. Metab., August 1, 2009; 94(8): 2841 - 2849. [Abstract] [Full Text] [PDF]

				D. S. Goldstein and C. Holmes Neuronal Source of Plasma Dopamine Clin. Chem., November 1, 2008; 54(11): 1864 - 1871. [Abstract] [Full Text] [PDF]

				M. N. Helms, J. Self, H. F. Bao, L. C. Job, L. Jain, and D. C. Eaton Dopamine activates amiloride-sensitive sodium channels in alveolar type I cells in lung slice preparations Am J Physiol Lung Cell Mol Physiol, October 1, 2006; 291(4): L610 - L618. [Abstract] [Full Text] [PDF]

				G. Eisenhofer, I. J. Kopin, and D. S. Goldstein Catecholamine Metabolism: A Contemporary View with Implications for Physiology and Medicine Pharmacol. Rev., September 1, 2004; 56(3): 331 - 349. [Abstract] [Full Text] [PDF]

				D. S. Goldstein, G. Eisenhofer, and I. J. Kopin Sources and Significance of Plasma Levels of Catechols and Their Metabolites in Humans J. Pharmacol. Exp. Ther., June 1, 2003; 305(3): 800 - 811. [Abstract] [Full Text] [PDF]

				C. A. Strott Sulfonation and Molecular Action Endocr. Rev., October 1, 2002; 23(5): 703 - 732. [Abstract] [Full Text] [PDF]

				M. W. H. Coughtrie and L. E. Johnston Interactions between Dietary Chemicals and Human Sulfotransferases{---}Molecular Mechanisms and Clinical Significance Drug Metab. Dispos., April 1, 2001; 29(4): 522 - 528. [Abstract] [Full Text]

				E. Eldrup and E. A. Richter DOPA, dopamine, and DOPAC concentrations in the rat gastrointestinal tract decrease during fasting Am J Physiol Endocrinol Metab, October 1, 2000; 279(4): E815 - E822. [Abstract] [Full Text] [PDF]

				P. Kreis, S. Brandner, M. W.H. Coughtrie, U. Pabel, W. Meinl, H. Glatt, and U. Andrae Human phenol sulfotransferases hP-PST and hM-PST activate propane 2-nitronate to a genotoxicant Carcinogenesis, February 1, 2000; 21(2): 295 - 299. [Abstract] [Full Text] [PDF]