中华心血管病杂志
中華心血管病雜誌
중화심혈관병잡지
Chinese Journal of Cardiology
2012年
5期
421-426
,共6页
董平栓%来利红%王红雷%邢适颖%朱继红%杨旭明%王绍欣%李转珍%尚喜燕
董平栓%來利紅%王紅雷%邢適穎%硃繼紅%楊旭明%王紹訢%李轉珍%尚喜燕
동평전%래리홍%왕홍뢰%형괄영%주계홍%양욱명%왕소흔%리전진%상희연
冠状血管%肌细胞,平滑肌%二十二碳六烯酸类%大电导钙激活钾通道%钾通道,电压门控
冠狀血管%肌細胞,平滑肌%二十二碳六烯痠類%大電導鈣激活鉀通道%鉀通道,電壓門控
관상혈관%기세포,평활기%이십이탄륙희산류%대전도개격활갑통도%갑통도,전압문공
Coronary vessels%Myocytes,smooth muscle%Docosahexaenoic acids%Large-conductance calcium-activated potassium channels%Potassium channels,voltage-gated
目的 探讨二十二碳六烯酸(DHA)对大鼠冠状动脉平滑肌细胞大电导钙激活性钾通道电流(IBKCa)和电压依赖性钾通道电流(IKv)的动力学影响,阐述DHA舒张血管的机制.方法 采用膜片钳技术在全细胞模式下,记录0、10、20、40、60和80 μmol/L的DHA对大鼠冠状动脉平滑肌细胞上IBKCa和IKv的影响.结果 (1)DHA可呈浓度依赖性地增加IBKCa和BKCa尾电流,对IBKCa稳态激活无影响.在指令电压+ 150 mV,不同浓度DHA(0、10、20、40、60和80μmol/L)作用下,IBKCa电流密度分别为(68.2±22.8)、(72.4±24.5)、( 120.4±37.9)、(237.5±53.2)、( 323.6±74.8)和(370.6±88.2) pA/pF(P<0.05,n=30).DHA对IBKCa的半效作用浓度(EC50)为(36.22±2.17)μmol/L.(2)DHA对IKv和Kv尾电流呈浓度依赖性抑制,使IKv稳态激活曲线右移、稳态失活曲线左移.在指令电压+ 50 mV,不同浓度DHA(0、10、20、40、60和80 μmol/L)作用下,IKv电流密度分别为(43.9±2.3)、(43.8±2.3)、(42.9±2.0)、(32.3±1.9)、(11.7±1.5)和(9.6±1.2) pA/pF(P<0.05,n=30).DHA对IKv的EC50为(44.19±0.63) μmol/L.结论 DHA对BKCa通道有激活作用,对Kv通道有抑制作用.DHA舒张血管的作用是对血管平滑肌细胞BKCa及Kv通道综合作用的结果.
目的 探討二十二碳六烯痠(DHA)對大鼠冠狀動脈平滑肌細胞大電導鈣激活性鉀通道電流(IBKCa)和電壓依賴性鉀通道電流(IKv)的動力學影響,闡述DHA舒張血管的機製.方法 採用膜片鉗技術在全細胞模式下,記錄0、10、20、40、60和80 μmol/L的DHA對大鼠冠狀動脈平滑肌細胞上IBKCa和IKv的影響.結果 (1)DHA可呈濃度依賴性地增加IBKCa和BKCa尾電流,對IBKCa穩態激活無影響.在指令電壓+ 150 mV,不同濃度DHA(0、10、20、40、60和80μmol/L)作用下,IBKCa電流密度分彆為(68.2±22.8)、(72.4±24.5)、( 120.4±37.9)、(237.5±53.2)、( 323.6±74.8)和(370.6±88.2) pA/pF(P<0.05,n=30).DHA對IBKCa的半效作用濃度(EC50)為(36.22±2.17)μmol/L.(2)DHA對IKv和Kv尾電流呈濃度依賴性抑製,使IKv穩態激活麯線右移、穩態失活麯線左移.在指令電壓+ 50 mV,不同濃度DHA(0、10、20、40、60和80 μmol/L)作用下,IKv電流密度分彆為(43.9±2.3)、(43.8±2.3)、(42.9±2.0)、(32.3±1.9)、(11.7±1.5)和(9.6±1.2) pA/pF(P<0.05,n=30).DHA對IKv的EC50為(44.19±0.63) μmol/L.結論 DHA對BKCa通道有激活作用,對Kv通道有抑製作用.DHA舒張血管的作用是對血管平滑肌細胞BKCa及Kv通道綜閤作用的結果.
목적 탐토이십이탄륙희산(DHA)대대서관상동맥평활기세포대전도개격활성갑통도전류(IBKCa)화전압의뢰성갑통도전류(IKv)적동역학영향,천술DHA서장혈관적궤제.방법 채용막편겸기술재전세포모식하,기록0、10、20、40、60화80 μmol/L적DHA대대서관상동맥평활기세포상IBKCa화IKv적영향.결과 (1)DHA가정농도의뢰성지증가IBKCa화BKCa미전류,대IBKCa은태격활무영향.재지령전압+ 150 mV,불동농도DHA(0、10、20、40、60화80μmol/L)작용하,IBKCa전류밀도분별위(68.2±22.8)、(72.4±24.5)、( 120.4±37.9)、(237.5±53.2)、( 323.6±74.8)화(370.6±88.2) pA/pF(P<0.05,n=30).DHA대IBKCa적반효작용농도(EC50)위(36.22±2.17)μmol/L.(2)DHA대IKv화Kv미전류정농도의뢰성억제,사IKv은태격활곡선우이、은태실활곡선좌이.재지령전압+ 50 mV,불동농도DHA(0、10、20、40、60화80 μmol/L)작용하,IKv전류밀도분별위(43.9±2.3)、(43.8±2.3)、(42.9±2.0)、(32.3±1.9)、(11.7±1.5)화(9.6±1.2) pA/pF(P<0.05,n=30).DHA대IKv적EC50위(44.19±0.63) μmol/L.결론 DHA대BKCa통도유격활작용,대Kv통도유억제작용.DHA서장혈관적작용시대혈관평활기세포BKCa급Kv통도종합작용적결과.
Objective To investigate the effects of docosahexaenoic acid (DHA) on large-conductance Ca2 + -activated K+ ( BKCa ) channels and voltage-dependent K+ ( Kv ) channels in rat coronary artery smooth muscle cells ( CASMCs ),and evaluate the vasorelaxation mechanisms of DHA.Methods BKCa and Kv currents in individual CASMC were recorded by patch-clamp technique in whole-cell configuration.Effects of DHA at various concentrations (0,10,20,40,60 and 80 μ mol/L) on BKCa and Kv channels were observed.Results ( 1 ) DHA enhanced IBKCa and BKCa tail currents in a concentration-dependent manner while did not affect the stably activated curves of IBKCa+ IBKCa current densities were (68.2±22.8),(72.4 ±24.5),(120.4 ±37.9),(237.5 ±53.2),(323.6 ±74.8) and (370.6 ±88.2 )pA/pF respectively (P < 0.05,n =30) with the addition of 0,10,20,40,60 and 80 μmol/L DHA concentration,and half-effect concentration ( EC50 ) of DHA was (36.22 ± 2.17 ) μmol/L.(2) IKv and Kv tail currents were gradually reduced,stably activated curves of IKv were shift to the right,and stably inactivated curves were shifted to the left in the presence of DHA.IKv current densities were (43.9 ±2.3),(43.8±2.3),(42.9±2.0),(32.3±1.9),(11.7±1.5) and (9.6 ±1.2)pA/pF respectively(P<0.05,n =30) post treatment with 0,10,20,40,60 and 80 μmol/L DHA under manding potential equal to +50 mV,and EC50 of DHA was (44.19 ±0.63) μmol/L.Conclusion DHA can activate BKCa channels and block Kv channels in rat CASMCs,the combined effects on BKCa and Kv channels lead to the vasodilation effects of DHA on vascular smooth muscle cells.