机体内环境理化因素对降钙素基因相关肽（CGRP）释放的影响

EFFECTS OF SOME PHYSICAL AND CHEMICAL FACTORS ON CGRP RELEASE FROM MESENTERIC ARTERIAL BED

我们以前的工作表明在内毒素和失血性休克时ＣＧＲＰ释放入血循环。本实验在离体大鼠肠系膜动脉床灌流的模型上，发现低ＰＨ、高乳酸、高氯化钠和高蔗糖溶液均能直接引起ＣＧＲＰ释放增加，进一步应用辣椒素预灌流，ＣＧＲＰ释放的作用被抑制，同时ＣＧＲＰ释放可以被一种钙引起的细胞内钙池释放阻断剂钉红所抑制，而且应用无钙的低ＰＨ，高乳酸及高渗液就不能引起ＣＧＲＰ释放增多，实验结果提示：上述理化因子导致ＣＧＲＰ从大鼠肠系膜动脉床的释放主要是通过刺激对辣椒素敏感的感觉神经，这一释放依赖于细胞外钙离子的存在以及Ｃａ２＋进入细胞引起的对钉红敏感的细胞内钙池Ｃａ２＋释放。

We have shown that calcitonin gene-related peptide (CGRP) is released into thecirculation during endotoxin or hemorrhagic shock.In the present study,it was observed that low pH, elevated levels of lactic acid,hypertonic NaCl and hypertonic sucrose caused CGRP release from isolated mesenteric arterial bed (MAB) of rat.All the responses were blocked when MAB was pretreated with capmicin. Ruthenium red,an inhibitor of Ca2+-induced Ca2+ release from intracellular Ca2+ pools, significantly inhibited the release of CGRP. In Ca2+free medium, low pH,lactic acid and hypertonic solutions became no longer capable of inducing the release of CGRP. The above results suggest that the observed release of CGRP in MAB was mediated by caopicin-sensitive sensory nerve endings, as a result of Ca2+-induced Ca2+ release from the intracellular Ca2+ store which is sensitive to ruthenium red.