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NEUROLOGY 1985;35:120
© 1985 American Academy of Neurology

Prostacyclin biosynthesis and platelet function in autonomic dysfunction

Michael R. Goldberg, MD, PhD, David Robertson, MD and Garret A. FitzGerald, MD

Division of Clinical Pharmacology, Departments of Medicine and Pharmacology, Vanderbilt University, Nashville, TN.

We measured urinary excretion of the principal metabolite of prostacyclin, PGI-M (2,3-dinor-6-keto-PGF1u) in two patients with Shy-Drager syndrome and three with idiopathic orthostatic hypotension. All patients had a rise in blood pressure (30 ± 6 mm Hg) after ingestion of 50 mg indomethacin. Urinary excretion of PGI-M was normal and fell 57 ± 11% after administration of indomethacin. In two subjects, there was no evidence of any circulating inhibitor of platelet aggregation when hypotension was induced by upright posture or ingestion of a meal. Despite the efficacy of indomethacin, these patients with autonomic dysfunction did not show increased production of the vasodilator prostanoid prostacyclin.

Address correspondence and reprint requests to Dr. Robertson, Pharmacology Department, Vanderbilt Medical Center, Nashville, TN 37232.

Dr. Goldberg was Clinical Associate Physician on the Elliot V. Newman Clinical Research Center. Dr. Robertson is the recipient of a Research Career Development Award from the National Institutes of Health. Dr. FitzGerald is the recipient of a Faculty Development Award from the Pharmaceutical Manufacturers Association Foundation. This work was supported by USPHS grants HL 30400, RR 0095, GM 31304 and GM 15431, and by a grant from the Hrafn Sveinbjarnarson Foundation.

Accepted for publication April 16, 1984.






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