α2-肾上腺素受体对大鼠肠系膜动脉床降钙素基因相关肽释放的调节作用

降钙素基因相关肽（CGRP）从感觉神经末梢的释放受多种机制的调节。本文在离体灌流的大鼠肠系膜动脉床组织上,利用药理学工具药,研究了α2-肾上腺素受体对CGRP的基础和内毒素刺激后释放的作用。结果发现,α2-受体激动剂UK14304（3×10－6mol／L）可以显著抑制CGRP的基础释放和内毒素（1～5μg／ml）刺激后的释放,抑制幅度为22％～42％;用α2-受体拮抗剂Yohimbine（10－5mol／L）可以完全阻断UK14304的作用。结果表明突触前α2-受体对CGRP从外周阻力血管组织的释放,尤其是内毒素刺激后的释放具有抑制作用,在内毒素休克晚期,α2-受体功能减低可能介导了外周组织CGRP的过量释放。

Modulatory action of alpha 2-adrenoceptor on calcitonin gene-related peptide release from rat mesenteric arterial bed

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.