牵张调控血管平滑肌细胞（VSMC）表型转变、增殖、迁移等功能，与动脉粥样硬化、血管成形术后再狭窄等疾病密切相关。中电导钙激活的钾通道（IKCa通道）主要表达于合成表型VSMC。研究证明，IKCa通道的表达和活性与VSMC的表型转变、增殖、迁移呈正相关。阻断该通道，可有效抑制动脉粥样硬化和血管成形术后再狭窄。尽管牵张和IKCa通道具有上述相似的功能，且IKCa通道为张力敏感通道，但目前对IKCa通道与牵张调控VSMC功能变化的关系没有任何报道。 鉴于此，本项目提出科学假设"病理性牵张通过上调IKCa通道表达、促进通道开放,进而激活相应的信号通路,促进VSMC表型转变、增殖和迁移。生理性牵张则相反"，并开展"IKCa通道在周期性牵张调控VSMC表型转变、增殖、迁移中的作用及机制研究"对上述假设进行验证，以期为深入理解周期性牵张调控VSMC功能变化的机制、找寻心血管疾病的治疗策略提供新依据。

Stretch influences the phenotype modulation, proliferation and migration of vascular smooth muscle cell (VSMC), further leads to some cardiovascular diseases, such as atherosclerosis and restenosis. Intermediate-conductance Ca2+-activated K+ (IKCa) channel mainly expresses in VSMC with synthetic phenotype, and its expression and activity are tightly related to the proliferation and migration of VSMC. It has been also demonstrated that the blockade of IKCa channel can decrease the development of atherosclerosis and restenosis. Furthermore, this channel is also stretch-sensitive. However, there is rare report on the relationship between the IKCa channel and VSMC function in response to stretch although they play some similar functions and shear some similar mechanisms as mentioned above. In view of this base, we rasie a scientific hypothesis "pathological stretch upregulates IKCa channel expression and promotes its activity, then actives the corresponding signal pathway, and further promotes VSMC phenotype modulation, proliferation and migration. Contrarily, phisological stretch behaves in a reverse way". To testfy this scientific hypothesis, the role and mechanism of IKCa channel in cyclic stretch-regulated phenotype modulation, proliferation and migration of VSMC will be explored in this project. This study aims to provide new insights into understanding the mechanism by which cyclic stretch influences the VSMC function and finding novel therapeutic strategy for cardiovascular disease.