Wu Z X, Han Q D, Bai Y, Wang X
Institute of Vascular Medicine, Beijing Medical University.
Sheng Li Xue Bao. 1995 Dec;47(6):573-9.
We have shown that calcitonin gene-related peptide (CGRP) is released into the circulation 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 capsaicin. Ruthenium red, an inhibitor of Ca(2+)-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 capsaicin-sensitive sensory nerve endings, as a result of Ca(2+)-induced Ca2+ release from the intracellular Ca2+ store which is sensitive to ruthenium red.
我们已经表明，降钙素基因相关肽（CGRP）在内毒素或失血性休克期间释放到循环中。在本研究中，观察到低pH、乳酸水平升高、高渗NaCl和高渗蔗糖可导致大鼠离体肠系膜动脉床（MAB）释放CGRP。当用辣椒素预处理MAB时，所有这些反应均被阻断。钌红是一种抑制Ca（2+）诱导的细胞内Ca2+库中Ca2+释放的抑制剂，可显著抑制CGRP的释放。在无Ca2+培养基中，低pH、乳酸和高渗溶液不再能够诱导CGRP的释放。上述结果表明，MAB中观察到的CGRP释放是由辣椒素敏感的感觉神经末梢介导的，这是Ca（2+）诱导的对钌红敏感的细胞内Ca2+储存中Ca2+释放的结果。
