Vasodilatation induced by capsaicin in rat mesenteric vessels is probably independent of nitric oxide synthesis

• Published in: Pharmacological research 1994-10, Vol.30 (3), p.253-261
• Main Authors: Potenza, M.A., De Salvatore, G., Montagnani, M., Serio, M., Mitolo-Chieppa, D.
• Format: Article
• Language: English
• Subjects: Amino Acid Oxidoreductases - antagonists & inhibitors; Animals; Arginine - analogs & derivatives; Arginine - pharmacology; calcitonin gene-related peptide (CGRP); Calcitonin Gene-Related Peptide - pharmacology; capsaicin; Capsaicin - antagonists & inhibitors; Capsaicin - pharmacology; Dose-Response Relationship, Drug; In Vitro Techniques; Male; NG-Nitroarginine Methyl Ester; nitric oxide (NO); Nitric Oxide - metabolism; Nitric Oxide Synthase; rat mesenteric vascular bed; Rats; Rats, Wistar; Splanchnic Circulation - drug effects; Vasodilation - drug effects
• ISSN: 1043-6618; 1096-1186
• DOI: 10.1016/1043-6618(94)80107-X

Vasal relaxation induced by capsaicin was investigated on perfused mesenteric vascular bed prepared from Wistar rats. Bolus infusion of capsaicin, from 3.5 to 16 nmol, elicited a dose-dependent vasal relaxation effect, which was antagonized by pretreatment with 3 × 10 −6 M calcitonin gene-related peptide (CGRP) (8–37), an antagonist of CGRP. In order to test whether NO-release is involved in vasorelaxant response to capsaicin, a preparation of mesenteric vascular bed was perfused and superfused for 1 h by N ω-nitro-L-arginine methyl ester (L-NAME) (3×10 −3 M), an NO-synthase inhibitor. Vasodilatation induced by capsaicin remained unchanged, while that induced by acetylcholine, used as control, was significantly reduced. The results indicate that in the mesenteric bed, capsaicin-induced vasodilatation is probably independent of the NO-synthesis mechanism and possibly mediated by CGRP.