CAJ | 학술논문

本研究采用全细胞膜片钳技术观察了SNCl62(一种选择性δ阿片受体激动剂)对人鼠心室肌细胞L型钙电流(L-type Ca2+current,ICa-L)和瞬时外向钾电流(transient outward K+current,Ito)的影响.结果显示,SNCl62明显抑制大鼠心室肌细胞,Ica+L和Ica+L,对Ica+L.和k的最大抑制率分别为(46.13±4.12)%和(36.53±10.57)%.1x10-4mol/L SNCl62使,Ica+L的甲均电流密度从(8.98±0.40)pA/pF下降到(4.84±0.44)pA/pF(P<0.01,n=5),Ito的平均电流密度从(18.69±2.42)pA/pF降低到(11.73±1.67)pA/pF(P<0.01,n=5).单独应用naltrindole(一种选择性δ阿片受体拮抗剂)对大鼠心室肌细胞Ica+L和Ito无显著作用,但预先应用naltrindole可以消除SNCl62对Ica+L和Ito的抑制作用.结果表明,通过δ阿片受体,SNCl62(1x10-6～1x10-4mol/L)浓度依赖性地抑制人鼠心室肌细胞Ica+L和Ito这可能是激动δ阿片受体产生抗心律失常效应的重要机制.
본연구채용전세포막편겸기술관찰료SNCl62(일충선택성δ아편수체격동제)대인서심실기세포L형개전류(L-type Ca2+current,ICa-L)화순시외향갑전류(transient outward K+current,Ito)적영향.결과현시,SNCl62명현억제대서심실기세포,Ica+L화Ica+L,대Ica+L.화k적최대억제솔분별위(46.13±4.12)%화(36.53±10.57)%.1x10-4mol/L SNCl62사,Ica+L적갑균전류밀도종(8.98±0.40)pA/pF하강도(4.84±0.44)pA/pF(P<0.01,n=5),Ito적평균전류밀도종(18.69±2.42)pA/pF강저도(11.73±1.67)pA/pF(P<0.01,n=5).단독응용naltrindole(일충선택성δ아편수체길항제)대대서심실기세포Ica+L화Ito무현저작용,단예선응용naltrindole가이소제SNCl62대Ica+L화Ito적억제작용.결과표명,통과δ아편수체,SNCl62(1x10-6～1x10-4mol/L)농도의뢰성지억제인서심실기세포Ica+L화Ito저가능시격동δ아편수체산생항심률실상효응적중요궤제.
In the present study,whole-cell patch-clamp technique was used to observe the effects of SNC162,a selective agonist of δ-opioid receptors,on L-type Ca2+current(Ica-L)and transient outward K+current(Ito)in rat ventricular myocytes.The results showed that SNC162 significantly inhibited Ica-L and Ito in rat ventricular myocytes.The maximal inhibition rate of Ica-L and Ito reached(46.13±4.12)% and(36.53±10.57)%,respectively.SNC162 at 1× 10-4 mol/L inhibited the current density of Ica-L from(8.98±0.40)pA/pF to(4.84±0.44) pA/pF(P<0.01,n=5)and inhibited that of Ito from(18.69±2.42)pA/pF to(11.73±1.67)pA/pF(P<0.01,n=5).Furthermore,the effects of naltrindole,a highly selective antagonist of δ-opioid receptors,on Ica-L and Ito were also observed.The results showed that naltrindole alone had no effects on Ica-L and Ito,while it abolished the inhibitory effects of SNC162 on Ica-L and Ito.In conclusion,SNC162 concentration-dependently inhibited Ica-L and Ito in rat ventricular myocytes via activation of the δ-opioid receptors,which may be a fundamental mechanism underlying the antiarrhythmic effect of activating δ-opioid receptors.