Potenza M A, De Salvatore G, Montagnani M, Serio M, Mitolo-Chieppa D
Institute of Pharmacology, Medical School, University of Bari, Italy.
Pharmacol Res. 1994 Oct-Nov;30(3):253-61. 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 x 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 omega-nitro-L-arginine methyl ester (L-NAME) (3 x 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.
在由Wistar大鼠制备的灌注肠系膜血管床中研究了辣椒素诱导的血管舒张作用。静脉注射3.5至16 nmol的辣椒素可引起剂量依赖性血管舒张效应，该效应可被用3×10⁻⁶ M降钙素基因相关肽（CGRP）拮抗剂（8 - 37）预处理所拮抗。为了测试一氧化氮（NO）释放是否参与辣椒素的血管舒张反应，用NO合酶抑制剂Nⁿ-硝基-L-精氨酸甲酯（L-NAME）（3×10⁻³ M）对肠系膜血管床制备物进行灌注和表面灌注1小时。辣椒素诱导的血管舒张保持不变，而用作对照的乙酰胆碱诱导的血管舒张则显著降低。结果表明，在肠系膜床中，辣椒素诱导的血管舒张可能独立于NO合成机制，并且可能由CGRP介导。
