Hua X Y, Jinno S, Back S M, Tam E K, Yaksh T L
Department of Anesthesiology, University of California, San Diego, La Jolla 92093.
Neuropharmacology. 1994 Oct;33(10):1147-54. doi: 10.1016/s0028-3908(05)80004-8.
Application of capsaicin (CAP), bradykinin (BK) or nicotine (NIC) to intraluminally perfused rat tracheas induced an increase in calcitonin gene-related peptide (CGRP) levels in the perfusates. Depletion of sensory afferent CGRP with systemic CAP pretreatment resulted in a significant reduction of CGRP release evoked by CAP, BK or NIC. Chemical destruction of sympathetic nerve fibres by systemic pretreatment with 6-hydroxydopamine reduced CGRP release evoked by NIC, but did not alter the release produced by CAP or BK. Elimination of the tracheal mast cell population by pretreatment with compound 48/80 did not alter the effects of CAP, BK or NIC. CGRP release evoked by BK and NIC, but not CAP, was diminished by indomethacin, suggesting that cyclooxygenase products mediate the actions of BK and NIC. Prostaglandins, PGE1, PGE2, PGF2 alpha and PGI2, displayed stimulatory effects on CGRP release in the trachea. There are evidently multiple mechanisms mediating CGRP release from sensory terminals in rat trachea. It appears that CAP exerts a direct action on sensory nerves, while the effects of BK and NIC are mediated by PG synthesis. Sympathetic activation may be involved in NIC, but not BK, induced PG-mediated CGRP release.
将辣椒素（CAP）、缓激肽（BK）或尼古丁（NIC）应用于经腔内灌注的大鼠气管，可导致灌注液中降钙素基因相关肽（CGRP）水平升高。全身应用CAP预处理使感觉传入神经的CGRP耗竭，导致由CAP、BK或NIC诱发的CGRP释放显著减少。全身用6-羟基多巴胺预处理对交感神经纤维进行化学破坏，可减少由NIC诱发的CGRP释放，但不改变由CAP或BK引起的释放。用化合物48/80预处理消除气管肥大细胞群体，不会改变CAP、BK或NIC的作用。吲哚美辛可减少由BK和NIC诱发的CGRP释放，但不影响由CAP诱发的释放，提示环氧化酶产物介导BK和NIC的作用。前列腺素PGE1、PGE2、PGF2α和PGI2对气管中CGRP的释放显示出刺激作用。显然有多种机制介导大鼠气管感觉神经末梢释放CGRP。似乎CAP对感觉神经发挥直接作用，而BK和NIC的作用是由PG合成介导的。交感神经激活可能参与由NIC而非BK诱导的PG介导的CGRP释放。
