title: Prostaglandins contribute to the vasodilation induced by nicotinic acid.
abstract: The significance of endogenously formed prostaglandins in the vasodilation induced by nicotinic acid (NIC) was investigated. The forearm venous plasma level of radioimmunoassayed PGE (R-PGE) and the forearm blood flow (FBF) were measured in 13 healthy male volunteers at rest and during infusion of NIC. Each subject was subsequently re-studied after pretreatment with the PG synthesis inhibitor, naproxen. In the absence of naproxen, NIC infusion resulted in an almost four-fold rise in the release of R-PGE and a 60% increase in FBF. Pretreatment with naproxen did not affect the basal release of R-PGE or the basal FBF but inhibited both the release of R-PGE and the increase in FBF following NIC. The data support the hypothesis that the vasodilating effect of NIC is largely dependent upon an increased vascular formation of PG.
mesh_terms: D000328:Adult; D002845:Chromatography; D005542:Forearm / Q000098:blood supply; D006801:Humans; D007275:Injections, Intravenous; D008297:Male; D009288:Naproxen / Q000494:pharmacology; D009539:Nicotinic Acids / Q000008:administration & dosage / Q000494:pharmacology*; D011448:Prostaglandin Antagonists / Q000494:pharmacology; D011453:Prostaglandins / Q000097:blood / Q000502:physiology*; D011458:Prostaglandins E / Q000097:blood / Q000378:metabolism / Q000502:physiology; D011863:Radioimmunoassay; D012636:Secretory Rate / Q000187:drug effects; D014664:Vasodilation / Q000187:drug effects*
chemical_list: D009539:Nicotinic Acids; D011448:Prostaglandin Antagonists; D011453:Prostaglandins; D011458:Prostaglandins E; D009288:Naproxen