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研究铅及蛋白激酶C的激活剂在收缩过程中对钙信号系统的影响。制各家兔肠系膜动脉血管条，悬吊于浴槽中．其张力变化经换能并放大后描记于记录仪上。实验中观察到leadacetate（10-10～10-3mol／L）能使之产生收缩（ED50为10－5mol／L）。这种收缩可被蛋白激酶C激动剂TPA及Mezarin加强而导致剂量反应曲线的左移。无活性的TPA缺乏此种作用。而蛋白激酶C的选择性抑制剂H7则可阻抑这种收缩。在无钙溶液中leadacetate不再引起动脉条的收缩。verapamil则可减低铅引起的收缩。去除血管内皮对铅收缩并无影响、本文表明铅引起的收缩与钙信号系统中蛋白激酶C这一环节有密切关系。
To investigate the effects of lead and protein kinase C activators on the calcium signaling system during contraction. System of rabbit rabbit mesenteric artery, suspended in the bath. The change of tension can be traced back to the recorder after being transduced and magnified. Leadacetate (10-10 ~ 10-3mol / L) was observed in the experiment to produce contraction (ED50 of 10-5mol / L). This contraction can be enhanced by the protein kinase C agonists TPA and Mezarin resulting in a shift to the left of the dose-response curve. Inactive TPA lacks this effect. The selective inhibitor of protein kinase C H7 can inhibit this contraction. Leadacetate no longer causes arterial constriction in calcium-free solutions. Verapamil can reduce lead-induced contraction. Removal of the vascular endothelium has no effect on lead contractions. This paper shows that lead-induced contractions are closely related to protein kinase C in the calcium signaling system.