Prostaglandins and nicotinate-provoked increase in cutaneous blood flow
- 1 September 1985
- journal article
- research article
- Published by Wiley in Clinical Pharmacology & Therapeutics
- Vol. 38 (3), 273-277
- https://doi.org/10.1038/clpt.1985.170
Abstract
The mechanism of topically applied methyl nicotinate-induced local cutaneous erythema was studied in normal human subjects. Aqeuous methyl nicotinate (0, 0.1, 10.0, and 100 mmol/L) was applied to the volar forearms in quadruplicate after oral pretreatments with 25 mg doxepin hydrochloride, 600 mg ibuprofen, 50 mg indomethacin, 975 mg aspirin, and lactose placebo. The cutaneous vascular response was monitored by laser Doppler velocimetry. Although doxepin did not affect the cutaneous vascular response to methyl nicotinate, indomethacin, ibuprofen, and aspirin significantly suppressed the response. Because indomethacin, ibuprofen, and aspirin have different chemical structures, the common property of inhibition of the response to methyl nicotinate may be assigned to their common pharmacologic action, i.e., inhibition of prostaglandin bioformation.This publication has 4 references indexed in Scilit:
- Noninvasive Assessment of Local Nicotinate Pharmacodynamics by PhotoplethysmographyJournal of Investigative Dermatology, 1983
- Aspirin blocks nicotinic acid–induced flushingClinical Pharmacology & Therapeutics, 1982
- Flushing Reactions: Consequences and MechanismsAnnals of Internal Medicine, 1981
- The Mechanism of Action of RubefacientsJournal of Investigative Dermatology, 1959