CAJ | 학술논문

　　目的：研究UTP对急性酶分离的猪冠状动脉平滑肌细胞上BKCa通道的作用，探讨PKC在其过程中的作用机制。方法：应用cell-attached技术记录急性酶分离的猪冠状动脉平滑肌细胞上BKCa电流。用pCLAMP10.0软件系统进行数据采集及分析。结果：在cell-attached膜片上,80μMUTP可明显激活BKCa通道(P＜0.05,n=21)。PLC抑制剂U73122可抑制UTP对BKCa的激活作用（P＜0.05, n=5）。 PKC激动剂PMA（10nM），可使BKCa通道开放概率明显降低（P＜0.05, n=9）。 UTP(80μM)预处理细胞之后，PKC特异性抑制剂Bis-Ⅰ(1μM),可使BKCa通道开放概率进一步增加（P＜0.05, n=9）。结论：在cell-attached膜片上，UTP经由PLC信使转导通路激活猪冠脉平滑肌细胞BKCa通道；PKC对此过程具有干预作用。
　　목적：연구UTP대급성매분리적저관상동맥평활기세포상BKCa통도적작용，탐토PKC재기과정중적작용궤제。방법：응용cell-attached기술기록급성매분리적저관상동맥평활기세포상BKCa전류。용pCLAMP10.0연건계통진행수거채집급분석。결과：재cell-attached막편상,80μMUTP가명현격활BKCa통도(P＜0.05,n=21)。PLC억제제U73122가억제UTP대BKCa적격활작용（P＜0.05, n=5）。 PKC격동제PMA（10nM），가사BKCa통도개방개솔명현강저（P＜0.05, n=9）。 UTP(80μM)예처리세포지후，PKC특이성억제제Bis-Ⅰ(1μM),가사BKCa통도개방개솔진일보증가（P＜0.05, n=9）。결론：재cell-attached막편상，UTP경유PLC신사전도통로격활저관맥평활기세포BKCa통도；PKC대차과정구유간예작용。
Objective: To study the effect of UTP on BKCa channels in porcine coronary artery smooth muscle cells, and explore the regulatory effect of PKC. Methods: The coronary artery was excised from the heart of porcine. All experiments were done on single smooth muscle cell isolated enzymatically in symmetric high potassium solution and currents were recorded by patch clamp single channel recording technique. pCLAMP10.0 software was used to record and analyze data. Results: In cell-attached patch, UTP (80 μM) enhanced BKCa channels open probability (Po) and reduced the mean close time (Tc) (P<0.01,n=21). In the presence of UTP, the specific blocker of phospholipase C -U73122 (10 μM) decreased BKCa channels Po (P<0.05,n=5). Application of PMA(10nM) obviously decreased BKCa channels Po(P<0.05,n=9). In the presence of UTP, Bis-Ⅰ(1μM) increased activation of BKCa channels (P<0.05,n=9). Conclusions: UTP can activate BKCa channels of porcine coronary ASMCs in cell-attached patches via PLC signal transduction pathway. PKC is involved in UTP mediated BKCa channels activation.