ISSN 0371-0874, CN 31-1352/Q

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α_(2)-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

孙威, 韩启德, 唐跃明, 王宪

北京医科大学第三医院血管医学研究所. 北京 100083

摘要

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。该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α_(2)-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,α_(2)-受体激动剂UK14304(3×10~(-6)mol/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α_(2)-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,α_(2)-受体功能减低可能介导了外周组织CGRP的过量释放。

关键词: 降钙素基因相关肽; α_(2)-肾上腺素受体; 内毒素

Modulatory action of a2-adrenoceptor on calcitonin gene-related peptide release from rat mesenteric arterial bed

Sun Wei, Han Qide, Tang Yueming, Wang Man

Institute of Vascular Medicine,Third Hospital,Beijing Medical University. Beijing 100083,China

Abstract

The release of calcitonin gene-related peptide (CGRP) from peripheral terminals of sensory nerves was modulated via multiple mechanisms. In the present study, pharmaological 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 UK14300 (3×10~(-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 presrpaptic #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.

Key words: Calcitonin gene-related peptide;#alpha#_(2)-adrenoceptor;Endotoxin

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引用本文:

孙威, 韩启德, 唐跃明, 王宪. α_(2)-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 [J]. 生理学报 1998; 50 (2): .

Sun Wei, Han Qide, Tang Yueming, Wang Man. Modulatory action of a2-adrenoceptor on calcitonin gene-related peptide release from rat mesenteric arterial bed. Acta Physiol Sin 1998; 50 (2): (in Chinese with English abstract).