内皮素对家犬肺静脉的作用机制

目的　观察内皮素 (ET) 3对肺静脉的张力改变并探讨其可能作用机制。方法　利用家犬离体肺静脉标本 ,记录药物对其张力的影响。结果　ET 3引起正常肺静脉的收缩反应 ;BQ12 3前处理可使其收缩反应明显减弱 (P <0 0 1) ,且对 30nmol·L-1ET 3的抑制作用趋近为零 (P <0 0 1) ,选择性ETB 受体阻断剂———IRL10 38对其ET 3的收缩反应无影响。BQ12 3前处理标本对 30mol·L-1ET 3表现出舒张反应 ,去掉内皮、另一选择性ETB 受体阻断剂———BQ788或一氧化氮合成酶抑制剂—左旋硝基精氨酸前处理对其舒张反应并无影响 ,而前列腺素内过氧化物合成酶抑制剂———消炎痛前处理可使其舒张反应明显减弱 (P <0 0 1)。IRL16 2 0亦引起肺静脉的收缩反应 ;IRL10 38前处理可使其收缩反应明显减弱 (P <0 0 1) ;去掉内皮或BQ12 3前处理对其收缩反应无影响。结论　在家犬肺静脉平滑肌上存在ETA 和ETB 两种受体 ,ET作用于此两种受体引起血管的收缩反应 ,在肺静脉平滑肌上还存在非ETA 非ETB 受体 ,ET作用于此受体通过释放舒张性前列腺素物质引起血管的舒张反应

Mechanism underlying endothelin-induced responses in canine isolated pulmonary veins

AIM To study mechanism of endothelin (ET) on canine pulmonary veins. METHODS The isometric tension of pulmonary venous strips was recorded. RESULTS ET 3 and IRL1640 produced contraction in pulmonary venous strips. ET 3 induced contraction was markedly suppressed by BQ123 (P<0 01). IRL1620 induced contraction was markedly suppressed by IRL1038(P<0 01). Under ET A receptor blockade, ET 3(30 nmol·L -1 ) produced endothelium independent relaxation, which was abolished by indomethacin (P<0 01 or 0 05)but neither by N G nitro L arginine nor BQ788, another selective ET B receptor antagonist. CONCLUSION The pulmonary venous responses to ET can be attributed mainly to activation of ET A and ET B receptors; ET A and ET B receptors located in venous smooth muscle mediated contractions. Non ET A/ non ET B receptors in the venous smooth muscle are likely to participate in prostaglandin mediated relaxation.