| 缝隙连接及其连接蛋白对血管加压素诱导的失血性休克大鼠血管收缩的作用研究 |
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| 引用本文： | 杨光明,彭小勇,周海军,李涛,刘良明.缝隙连接及其连接蛋白对血管加压素诱导的失血性休克大鼠血管收缩的作用研究[J].中国现代应用药学,2018,35(1):5-9. |
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| 作者姓名： | 杨光明 彭小勇 周海军 李涛 刘良明 |
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| 作者单位： | 第三军医大学大坪医院野战外科研究所,第三军医大学大坪医院野战外科研究所,第三军医大学大坪医院野战外科研究所,第三军医大学大坪医院野战外科研究所,第三军医大学大坪医院野战外科研究所 |
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| 基金项目： | 国家自然科学基金项目（面上项目）,军队“十三五”重大项目，国家教育部回国人员科研启动基金 |
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| 摘 要： | 摘要：目的 观察缝隙连接（GJ）及其组成亚单位连接蛋白（Cx）在血管加压素（AVP）诱导失血性休克大鼠血管收缩中的作用。方法 采用失血性休克大鼠模型和缺氧培养血管平滑肌细胞（VSMC），观察GJ阻断剂CBX和octanol、以及各Cx亚型反义寡核苷酸（AODN）对AVP诱导的血管收缩反应的影响，随后进一步观察参与AVP作用的Cx37和Cx43对AVP调节休克血管钙敏感性和缺氧VSMC内钙离子浓度的影响。结果 GJ阻断剂CBX和octanol明显抑制了AVP诱导的休克血管的收缩反应。在所有血管中表达的连接蛋白中，Cx37AODN和Cx43AODN明显抑制了AVP的血管收缩作用。进一步结果显示，Cx43AODN、而不是Cx37AODN，可拮抗AVP升高休克血管钙敏感性的作用。此外， AVP处理和干扰Cx37及Cx43对缺氧VSMC内钙离子浓度无明显影响。结论 缝隙连接在休克后AVP介导的血管收缩调节中有重要作用，Cx37和Cx43参与了这一过程，其中Cx43可能通过影响AVP介导的血管钙敏感性调节途径来发挥作用，而Cx37可能通过其它机制来参与AVP的血管调节作用。
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| 关 键 词： | 失血性休克 血管加压素 缝隙连接 连接蛋白 |
| 收稿时间： | 2017/6/26 0:00:00 |
| 修稿时间： | 2017/9/4 0:00:00 |
Roles of Gap Junctions and Its Connexins in Vasopressin-induced Vasoconstriction After Hemorrhagic Shock |
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| YANG Guangming,PENG Xiaoyong,ZHOU Haijun,LI Tao and LIU Liangming.Roles of Gap Junctions and Its Connexins in Vasopressin-induced Vasoconstriction After Hemorrhagic Shock[J].The Chinese Journal of Modern Applied Pharmacy,2018,35(1):5-9. |
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| Authors: | YANG Guangming PENG Xiaoyong ZHOU Haijun LI Tao and LIU Liangming |
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| Institution: | Research Institute of Surgery, Daping Hospital, The Third Military Medical University,Research Institute of Surgery, Daping Hospital, The Third Military Medical University,Research Institute of Surgery, Daping Hospital, The Third Military Medical University,Research Institute of Surgery, Daping Hospital, The Third Military Medical University,Research Institute of Surgery, Daping Hospital, The Third Military Medical University |
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| Abstract: | ABSTRACT: OBJECTIVE To investigate the role of gap junctions (GJs) and the GJ channel protein connexins (Cxs) in arginine vasopressin (AVP)-induced vasoconstriction after hemorrhagic shock. METHODS With superior mesenteric arteries (SMAs) from hemorrhagic-shock rats and hypoxia-treated vascular smooth muscle cells (VSMCs), the effects of GJ blockers CBX and octanol, and the antisense oligodeoxynucleotides (AODNs) of Cxs on the vascular effects of AVP after shock, and the effects of Cx37 and Cx43 on AVP-regulating the calcium sensitivity of SMAs after shock and intracellular calcium concentration in VSMCs after hypoxia were observed. RESULTS Blockade of GJs signi?cantly decreased the contractile response of SMAs to AVP after shock. Among all connexins that expressed in vessels, the AODNs of Cx37 and Cx43 significantly inhibited the vascular contractile effect of AVP after shock. Furthermore, Cx43AODN, but not Cx37AODN, significantly antagonized the AVP-induced increase of the calcium sensitivity of SMAs after shock. AVP treated or silencing of Cx37 and Cx43 had no significant influences on the intracellular calcium concentration in hypoxic VSMCs. CONCLUSION Gap junctions played an important role in AVP-mediated vascular contractile effect after hemorrhagic shock. Cx43 and Cx37 are the main isoforms of connexin involved. Cx43 plays effect mainly through AVP-mediated calcium sensitization pathway, while Cx37 may be through other mechanisms. |
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| Keywords: | hemorrhagic shock arginine vasopressin gap junctions connexin |
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