Sun W, Han Q D, Tang Y M, Wang X
Institute of Vascular Medicine, Third Hospital, Beijing Medical University, Beijing 100083.
Sheng Li Xue Bao. 1998 Apr;50(2):227-31.
The release of calcitonin gene-related peptide (CGRP) from peripheral terminals of sensory nerves was modulated via multiple mechanisms. In the present study, pharmacological agents were used to investigate the modulatory action of alpha 2-adrenoceptor on endotoxin-induced CGRP release from isolated perfused rat mesenteric arterial bed. The results showed that UK14304 (3 x 10(-6) mol/L), a potent alpha 2-adrenoceptor agonist, significantly inhibited both basal and endotoxin-induced CGRP release by 22%-42%, while specific antagonist of alpha 2-adrenoceptor yohimbine (10(-5) mol/L) blocked the effect of UK14304 completely. The data suggest that presynaptic alpha 2-adrenoceptor has an inhibitory effect on basal and endotoxin-induced CGRP release. Dysfunction of alpha 2-adrenoceptor in the late stage of endotoxic shock may be involved in the excess release of CGRP from the peripheral nerves.
感觉神经外周终末降钙素基因相关肽（CGRP）的释放受多种机制调节。在本研究中，使用药理学试剂研究α2 -肾上腺素能受体对内毒素诱导的离体灌注大鼠肠系膜动脉床CGRP释放的调节作用。结果显示，强效α2 -肾上腺素能受体激动剂UK14304（3×10(-6) mol/L）可显著抑制基础及内毒素诱导的CGRP释放达22% - 42%，而α2 -肾上腺素能受体特异性拮抗剂育亨宾（10(-5) mol/L）可完全阻断UK14304的作用。数据表明，突触前α2 -肾上腺素能受体对基础及内毒素诱导的CGRP释放具有抑制作用。内毒素休克后期α2 -肾上腺素能受体功能障碍可能与外周神经CGRP释放过多有关。
