中文摘要：

目的研究蛋白激酶A（PKA）、蛋白激酶G（PKG）、蛋白激酶C（PKC）在连接蛋白Cx40、Cx43调节缺氧处理大鼠肠系膜上动脉（SMA）内膜依赖的收缩反应性中的作用。方法以SD大鼠SMA为研究对象,用Cx40或Cx43的反义寡脱氧核苷酸（AODN）阻断SMA的Cx40或Cx43表达,观察缺氧处理SMA内膜依赖的收缩反应性的变化,以PKA、PKG、PKC特异性激动剂或拮抗剂改变相关信号通路,观察缺氧SMA在肌球蛋白轻链激酶（MLCK）活性、肌球蛋白轻链磷酸酶（MLCP）活性和内膜依赖的收缩反应性等方面的变化。结果杨梅黄酮（myricetin）、Cx40/43 AODN对常氧和缺氧血管的MLCK活性无明显影响;Cx40 AODN可以降低常氧血管和缺氧血管的MLCP活性,增加内膜依赖的血管收缩反应性;Cx43 AODN可以增加血管的MLCP活性,抑制血管内膜依赖的收缩反应性。8-Br-cAMP（PKA激动剂）、8-Br-cGMP（PKG激动剂）和staurosporine（PKC抑制剂）可以明显增加Cx40/43 AODN处理血管的MLCP活性,降低血管的收缩反应性;H-89（PKA抑制剂）、KT-5823（PKG抑制剂）和PMA（PKC激动剂）可以明显降低Cx40/43 AODN处理血管的MLCP活性,增加Cx40/43 AODN处理血管的收缩反应性。结论 Cx40和Cx43可以通过调节血管MLCP的活性,进而参与了休克血管钙敏感性和血管内膜依赖的收缩反应性的调节,

英文摘要：

Objective To investigate the mechanism of Cx40/43 regulating the endothelium-dependent vascular contractile reactivity after hypoxia.Methods With superior mesenteric arteries（SMAs）from rats treated by hypoxia,Cx40/43 antisense oligodeoxyribonucleotide（Cx40/43 AODN）and the specific activators or inhibitors to PKA,PKG and PKC,the changes of myosin light chain kinase′s（MLCK′s）activity,myosin light chain phosphatase′s（MLCP′s）activity and the endothelium-dependent contractile response of hypoxia treated SMA were observed.Results Cx40 AODN decreased the activity of MLCP,but increased the endothelium-dependent contractile response.Cx43 AODN increased the activity of MLCP,but decreased the endothelium-dependent contractile response.8-Br-cAMP（PKA activator）,8-Br-cGMP（PKG activator）and staurosporine（PKC inhibitor）significantly increased the activity of MLCP,but decreased the endothelium-dependent contractile response of SMAs treated by Cx40/43 AODN.H-89（PKA inhibitor）,KT-5823（PKG inhibitor）and PMA（PKC activator）significantly decreased the activity of MLCP,but increased the endothelium-dependent contractile response of SMAs treated by Cx40/43 AODN.Conclusion The possible mechanism that Cx40/43 regulates endothelium-dependent vasoconstrictor reactivity following hemorrhagic shock may be related to the PKA,PKG and PKC signal pathway.