Prostaglandins contribute to the vasodilation induced by nicotinic acid.
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.
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*
D009539:Nicotinic Acids; D011448:Prostaglandin Antagonists; D011453:Prostaglandins; D011458:Prostaglandins E; D009288:Naproxen