脑啡肽对离体动脉条收缩活动的影响及其机制分析

EFFECT OF ENKEPHALIN ON CONTRACTIVE ACTIVITY OF ARTERY STRIPS IN VITRO AND ANALYSIS OF ITS MECHANISM

亮氨酸脑啡肽(L-ENK)和甲硫氨酸脑啡肽(M-ENK)对兔耳动脉条在电场刺激下所产生的收缩反应具有抑制作用,此抑制效应具有剂量依赖关系,并且可以被阿片受体阻断剂纳洛酮阻断。用荧光法测定动脉条去甲肾上腺素(NE)释放量的实验表明,脑啡肽(ENK)是通过抑制支配动脉壁交感神经末梢释放NE,继而抑制血管平滑肌收缩的。实验还证明,吗啡对动脉条的收缩无抑制作用,从而表明在兔耳动脉上以δ亚型阿片受体为主,可能无μ亚型阿片受体。可卡因和育亨宾通过不同的作用途径使动脉条释放NE增加。

Contraction of the artery strips of rabbit ear induced by electric field stimulation was inhibited significantly after administration of Leu-enkephalin (L-ENK) or Metenkephalin (M-ENK). Concentration-dependent effect of L-ENK and M-ENK was observed. The inhibitory effect of ENK could be blocked completely by naloqone. Content of norepinephrin (NE) in the bath medium of artery strip was measured by fluorimetric assay. NE in the medium decreased significantly after pretreatment of the artery strips with L-ENK and M-ENK. These results suggested that enkephalins inhibited the contraction of artery smooth muscles probably by decreasing the release of NE from sympathetic nerve terminals. Experiments also proved that morphine, a ligand, acting predominantly at the opioid receptor of the μ-subtype, had no inhibitory effect on the contraction of ear artery strips, indicating that rabbit ear artery possesses opioid receptors of the δ-, but not the μ-subtype. Cocaine and yohimbine increased the release of NE from artery strips probably through a different course of action.