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Research Article Free access | 10.1172/JCI108866

Catecholamine Uptake, Accumulation, and Release in Acute Porphyria

M. Flint Beal, Nuzhet O. Atuk, Thomas C. Westfall, and Suzanne M. Turner

Department of Internal Medicine, University of Virginia School of Medicine, Charlottesville, Virginia 22901

Department of Pharmacology, University of Virginia School of Medicine, Charlottesville, Virginia 22901

Find articles by Beal, M. in: JCI | PubMed | Google Scholar

Department of Internal Medicine, University of Virginia School of Medicine, Charlottesville, Virginia 22901

Department of Pharmacology, University of Virginia School of Medicine, Charlottesville, Virginia 22901

Find articles by Atuk, N. in: JCI | PubMed | Google Scholar

Department of Internal Medicine, University of Virginia School of Medicine, Charlottesville, Virginia 22901

Department of Pharmacology, University of Virginia School of Medicine, Charlottesville, Virginia 22901

Find articles by Westfall, T. in: JCI | PubMed | Google Scholar

Department of Internal Medicine, University of Virginia School of Medicine, Charlottesville, Virginia 22901

Department of Pharmacology, University of Virginia School of Medicine, Charlottesville, Virginia 22901

Find articles by Turner, S. in: JCI | PubMed | Google Scholar

Published November 1, 1977 - More info

Published in Volume 60, Issue 5 on November 1, 1977
J Clin Invest. 1977;60(5):1141–1148. https://doi.org/10.1172/JCI108866.
© 1977 The American Society for Clinical Investigation
Published November 1, 1977 - Version history
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Abstract

Hypertension and tachycardia are well known features of acute porphyria and have been shown to be related to increased circulating catecholamines. The mechanism by which circulating catecholamines are increased was studied using the isolated perfused rat heart and human platelets as a model of adrenergic neuronal function. It was found that neither δ-aminolevulinate (ALA) nor porphobilinogen (PBG) blocked uptake or caused release in the isolated perfused rat heart. Platelets from six patients with acute prophyria, three in remission and three latent, with matching normal controls were studied with regard to their uptake of [3H]norepinephrine in the presence of ALA or PBG. It was found that ALA and PBG significantly reduced uptake and accumulation of [3H]-norepinephrine in patients with acute porphyria; however, no similar reduction in uptake and accumulation was observed in the platelets of normal controls. Therefore, it appears that there is a latent defect in the catecholamine uptake and (or) accumulation of platelets of patients with acute prophyria which only manifests itself in the presence of ALA or PBG. If platelet uptake serves as a model of adrenergic neuron uptake, this suggests that elevated circulating catecholamine levels during acute attacks of acute porphyria are caused at least partially by blockade of re-uptake into the sympathetic neurons.

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