中文摘要：

目的探讨精氨酸血管加压素（AVP）对缺氧血管平滑肌细胞（VSMC）中PKC—α、δ和ε亚型蛋白表达的调节作用及其可能机制。方法取50只Wistar大鼠的血管进行原代VSMC培养，观察AVP对缺氧VSMC胞质和胞膜成分中PKC-α、δ和ε亚型蛋白表达的影响，同时检测缺氧VSMC中3种磷脂酶（PLC、PLD、PLA，）的活性变化及AVP和PKC亚型抑制剂对其的作用。结果缺氧后VSMC胞膜成分中PKC—α和ε亚型的表达分别升高为正常组的1．5和2．0倍，而胞质成分中表达降低，AVP处理进一步升高胞膜PKC—α和ε亚型的表达（分别为正常组的2．4和2．6倍，P〈0．05）；而胞质和胞膜PKC-δ亚型有相似的变化趋势，但差异无统计学意义。同时，缺氧后PLC和PLD活性升高，AVP处理使PLC和PLD的活性进一步升高为正常组的1．6和2．1倍；PKC—α抑制剂G66976预处理可拮抗AVP诱导PLD活性升高的作用（PLD活性降低为AVP组的40．8％），而PKC-δ和ε抑制剂无明显作用；各组PLA2活性差异无统计学意义。结论AVP可通过促进VSMC胞质中的PKC-α和ε亚型向胞膜转位而激活，进而调节休克后血管反应性；PLC和PLD可能参与了AVP介导的PKC激活过程。

英文摘要：

Objective To observe the effect of arginine vasopressin （AVP） on the expression of PKC-α, δ and ε isoforms of vascular smooth muscle cell （ VSMC ） after hypoxia and its mechanisms. Methods With cultured VSMC from 50 Wistar rats,the effect of AVP on the expression of PKC-α,δ and ε isoforms in the cytosol and particulate fractions of VSMC after hypoxia were observed. At the same time, the activity of phospholipase C （ PLC ）, phospholipase D （ PLD ）, phospholipase A2 （ PLA2 ） and the effects of AVP and PKC isoform inhibitors were also observed. Results The expression of particulate PKC-α and increased about 1.5 and 2.0 folds, respectively after 90-min hypoxia, with a concomitant decrease in cytosolic fractions. AVP treatment further increased expression of PKC-α and e in the particulate fractions to 2.4 and 2.6 folds （ P 〈 0.05 ）. While PKC-δ showed a similar changes in the particulate and cytosolic fractions during the process, but there were no statistical differences among the groups. At the same time, treatment with hypoxia for 1.5 h caused a significant increase in PLC and PLD activity, AVP further increased of PLC and PLD activity to 1.6 and 2.1 folds, PKC-α inhibitor Go 6976 antagonized AVP-induced increased in PLD activity,which reduced to 40.8% as compared to AVP alone group. The PLA2 activity had no significant changes among the groups. Conclusion AVP improved vascular reactivity following shock through translocating PKC-α and e isoforms from a cytosol to a particulate and activation. And PLC and PLD may participate in the signal transduction pathway induced by AVP.