Scott T M, Chafe L
Faculty of Medicine, Memorial University of Newfoundland, St. John's, Canada.
Artery. 1994;21(1):38-50.
Earlier work on peptidergic fibres suggested some involvement of CGRP perivascular nerve fibres in acetylcholine-induced endothelium-dependent vascular relaxation. We have investigated the effect of blocking CGRP receptors and CGRP replacement on acetylcholine-induced endothelium-dependent vascular relaxation in the isolated perfused mesenteric arterial bed in normal Sprague-Dawley rats and in rats seven days following freeze-denervation of the superior mesenteric artery. Freeze-denervation was carried out under pentobarbital anesthesia (40 mg/Kg). It was found that the ability of acetylcholine to cause relaxation was reduced by CGRP receptor blocking with CGRP8-37 in vessels from control rats, but returned to pre-blocking levels after washout of the antagonist. Treatment with CGRP increased the relaxation due to acetylcholine in denervated vessel beds, but not in control tissues. The CGRP receptor appears to be involved in the acetylcholine-induced relaxation of blood vessels. The mechanism of action is not known, although both acetylcholine and CGRP, act through activation of K+ channels, and CGRP may facilitate the activation of K+ channels by acetylcholine.
早期关于肽能纤维的研究表明，降钙素基因相关肽（CGRP）血管周围神经纤维在乙酰胆碱诱导的内皮依赖性血管舒张中发挥了一定作用。我们研究了在正常斯普拉格-道利大鼠以及肠系膜上动脉冷冻去神经7天后的大鼠中，阻断CGRP受体和补充CGRP对乙酰胆碱诱导的离体灌注肠系膜动脉床内皮依赖性血管舒张的影响。冷冻去神经手术在戊巴比妥麻醉（40mg/Kg）下进行。结果发现，在对照大鼠的血管中，用CGRP8 - 37阻断CGRP受体会降低乙酰胆碱引起舒张的能力，但在拮抗剂洗脱后恢复到阻断前水平。用CGRP处理可增加去神经血管床中由乙酰胆碱引起的舒张，但对照组织中无此现象。CGRP受体似乎参与了乙酰胆碱诱导的血管舒张。其作用机制尚不清楚，尽管乙酰胆碱和CGRP均通过激活钾通道发挥作用，且CGRP可能促进乙酰胆碱对钾通道的激活。
