肺血管内皮细胞对交感神经末梢去甲肾上腺素释放的影响  

The Modulation of Release of Norepinephrine from Pulmonary Vascular Sympathetic Nerve Endings by Pulmonary Endothelium

作　　者：谢剑鸣[1] 薛全福[1] 

机构地区：[1]中国医学科学院基础医学研究所病理生理研究室

出　　处：《基础医学与临床》1994年第6期30-34,共5页Basic and Clinical Medicine

摘　　要：ｃＧＭＰ升高抑制肾上腺能神经末梢释放去甲肾上腺素（ＮＥ），内皮细胞释放的舒张因子（ＥＤＲＦ）增加ｃＣＭＰ，故其对交感神经ＮＥ的释放可能有调节作用。本文观察去内皮细胞或抑制ＥＤＲＦ合成后肺血管对跨膜交感神经刺激（ＴＮＳ）的反应及对２－［１４Ｃ］－ＮＥ的摄取和释放。利用磨擦损伤内皮细胞后或使用ＬＮＭＭＡ抑制ＥＤＲＦ合成后，肺血管对ＴＮＳ刺激的反应明显增加。尤以低频率刺激为甚。肺血管对２－［１４Ｃ］－ＮＥ的摄取无显著变化，但ＮＥ的释放却因去内皮而显著增高。利用猪的胸主动脉做为ＥＤＲＦ供体，其含有ＥＤＲＦ的流出液可以明显抑制去内皮的肺血管对ＴＮＳ的收缩反应及ＮＥ的释放。结果表明血管内皮细胞对肺动、静脉交感神经释放ＮＥ具有抑制作用。he release of norepinephrine(NE) from sympathetic nerve endings is inhi-bited by substances which raise cyclic 3',5'-guanosine monophosphate(cGMP)inneural tissue,EDRF elevates cGMP in vascular smooth muscle. Thus,EDRF mayalso modulate the release of norepinephrine(NE)from sympathetic nerves. Wetested the postulate with superfusion and measurement of 2-[14C]-NE effluxduring SNS at 0. 5 to 32 Hz in canine pulmonary arteries(PA)and veins(PV).Endothelium rubbing or N-L-monomethyl-arginine( LNMMA) ,an inhibitor ofEDRF synthase ,enhanced the efflux of 2-[14C]-NE from PA and PV and thecontractions to nerve stimulation when compared to artery and vein with intactendothelium,EDRF released from porcine thoracic aorta under basal conditionsinhibited the efflux of 2-[14C]-NE from artery and vein,The data support theconclusion that the endothelium can inhibit the release of NE from sympatheticnerves innervating canine pulmonary artery and vein.

关 键 词：内皮细胞 交感神经 去甲肾上腺素 肺血管 

分 类 号：Q577[生物学—生物化学]