Prostacyclin biosynthesis and platelet function in autonomic dysfunction.
We measured urinary excretion of the principal metabolite of prostacyclin, PGI-M (2,3-dinor-6-keto-PGF1 alpha) 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.
D015121:6-Ketoprostaglandin F1 alpha / Q000031:analogs & derivatives* / Q000096:biosynthesis / Q000652:urine; D000368:Aged; D001342:Autonomic Nervous System Diseases / Q000188:drug therapy / Q000378:metabolism* / Q000652:urine; D005260:Female; D006801:Humans; D007024:Hypotension, Orthostatic / Q000188:drug therapy / Q000378:metabolism* / Q000652:urine; D007213:Indomethacin / Q000494:pharmacology; D008297:Male; D008875:Middle Aged; D010974:Platelet Aggregation / Q000187:drug effects; D012791:Shy-Drager Syndrome / Q000188:drug therapy / Q000378:metabolism* / Q000652:urine
D015121:6-Ketoprostaglandin F1 alpha; C028290:2,3-dinor-6-ketoprostaglandin F1alpha; D007213:Indomethacin