参松养心胶囊对心室肌细胞钾通道的影响

目的观察参松养心胶囊干粉提取溶液对大鼠单个心室肌细胞内向整流钾电流(IK1)、瞬时外向钾电流(Ito)以及豚鼠心肌细胞延迟整流钾电流(Ik)的影响。方法用酶解法分离单个心室肌细胞,并用全细胞膜片钳记录技术。结果当药物浓度0.5%时,可以使大鼠心肌细胞IK1内向成分降低,使-100mV时IK1电流密度从(-10.8±1.8)pA/pF降至(-7.2±2.1)pA/pF,平均抑制率为(33.1±16.9)%(n=11,P<0.05),但不改变电流的翻转电位及整流特性。药物同时对Ito电流的瞬时成分有抑制作用,60mV时Ito电流密度从(-19.8±7.1)pA/pF降至(-10.0±3.9)pA/pF,平均抑制率为(50.6±10.8)%(n=6,P<0.05),稳态失活曲线左移,失活后恢复时间常数增大。药物浓度0.5%时,对Ik有电压依赖性抑制作用,50mV时对尾电流峰值的抑制率为(30.8±1.1)%(n=5,P<0.05)。结论参松养心胶囊干粉提取溶液对IK1,Ito和Ik均具有不同程度的阻滞作用。这种多离子通道阻滞作用不仅使参松养心胶囊具有广谱的抗心律失常疗效,减少致心律失常的副作用,对Ito的阻滞效应还将显示其独特的抑制2相折返的作用,值得对其作更深入和广泛的研究。     

槲寄生黄酮苷对大鼠心室肌细胞钾离子通道的作用

目的观察槲寄生黄酮苷对大鼠心室肌细胞钾离子通道的作用,探讨槲寄生黄酮苷抗心律失常作用机制。方法应用全细胞膜片钳技术记录槲寄生黄酮苷对大鼠单个心室肌细胞内向整流钾电流(IK1)、瞬时外向钾电流(Ito)的影响。结果应用50μg/ml和250μg/ml两种浓度的槲寄生黄酮苷分别使大鼠单个心室肌细胞内向整流钾电流(IK1)在实验电压-120mV时从给药前(-26.23±9.52)pA/pF减少到(-20.82±7.88)pA/pF,(-18.11±7.89)pA/pF(n=7,P<0.05);使大鼠心室肌细胞瞬时外向钾电流(Ito)在实验电压+50mV时,从给药前(26.14±6.67)pA/pF减少到(16.41±6.23)pA/pF,(13.25±3.78)pA/pF(n=4,P<0.05)。结论槲寄生黄酮苷抑制大鼠心室肌细胞IK1,Ito可能是其抗心律失常作用的一个机制。     

自发性高血压大鼠左心室肌细胞电生理研究

目的　研究自发性高血压大鼠 (SHR)左心室肌细胞的电生理特性。方法　以正常血压Wistar大鼠左心室肌细胞作为对照 ,采用玻璃微电极技术记录动作电位 ,应用膜片钳全细胞技术记录膜离子流 ,观察SHR左心室肌细胞动作电位及膜离子流的改变。结果　①SHR和Wisar大鼠的心脏 /体重比分别为 5 .6 6± 0 .46mg/g(n =2 0 )和 3.7± 0 .2 9mg/g(n =2 8) (P <0 .0 0 1) ,平均细胞膜电容分别为 2 80 .6 8± 6 7.98pF(n =91)和 189.94± 5 6 .5 9pF(n =137) (P <0 .0 5 )。②SHR左心室肌细胞动作电位时程较Wistar大鼠明显延长 [APD50 :2 1.33± 1.5 6ms(n =6 ) ,vs 14.91± 2 .95ms(n =11) ,P <0 .0 0 1;APD90 :16 4.6 7± 4ms ,vs 93.2 7± 10 .5 9ms ,P <0 .0 0 1]。③内向电流 :SHR左心室肌细胞的ICa -L密度与Wistar大鼠间无差异 [6 .93± 1.71pA/pF(n =2 0 ) ,vs 6 .19± 2 .85pA/pF(n =37) ],但前者的慢失活时间常数显著延长 (5 6 .0 1± 13.36ms,vs 43.6 3± 17.89ms,P <0 .0 0 1)。SHR左心室肌细胞的INa密度与Wistar大鼠间无差异 [2 4.6 1± 6 .72 pA/pF(n =16 ) ,vs 2 4.95± 6 .99pA/pF(n =18) ]。④外向电流 :SHR左心室肌细胞IK1内向电流密度显著小于Wistar大鼠 [- 12 0mV时 ,11.3± 2 .2 6 pA/pF(n =17) ,v     

MiRP1对异源转染的CHO细胞上HCN1和HCN2通道电生理特性的调节

目的 评价Mink相关肽1(MiRP1)对异源转染的CHO细胞上的HCN1、HCN2通道电生理特性的影响.方法 将MiRP1质粒DNA分别和HCN1、HCN2质粒DNA共转染CHO-K1细胞,用全细胞膜片钳记录细胞膜上的HCN通道电流.结果 MiRP1显著增加HCN2 [(37.8±4.8) pA/pF(n=11) vs (25.9±1.7) pA/pF(n=10); -140 mV, P<0 05]的电流密度,但是对HCN1的电流大小没有影响[(41.3±10.9) pA/pF(n=13) vs (34.9±7.8) pA/pF(n=11); P>0 05];MiRP1可加快HCN1[时间常数:(180.9±8.6) ms vs (306.1±45.6) ms; -80 mV, P<0 05]和HCN2 [时间常数:(391.8±33.6) ms vs (763.5±106.1) ms; -80 mV, P<0 05]激活动力学;MiRP1对HCN1及HCN2通道激活的电压依赖性没有影响.结论 MiRP1可加快HCN1和HCN2通道激活,且增加HCN2的电流表达.     

淫羊藿苷对兔心室肌细胞L-型钙电流的影响

目的:利用膜片钳技术研究淫羊藿苷(ICA)对兔单个心室肌细胞L-型钙电流(ICa,L)的影响。方法:采用酶解法分离兔单个心室肌细胞,应用全细胞膜片钳技术观察10,20,40μmol/L的ICA对心室肌细胞ICa,L的作用。结果:①10,20,40μmol/L的ICA使兔心室肌细胞ICa,L最大峰电流密度从(15.81±1.23)pA/pF分别降至(11.27±0.89)pA/pF,(9.48±0.85)pA/pF和(6.87±0.81)pA/pF(n=6,P<0.05),抑制率分别为28.7%,40.0%和56.5%;ICA使ICa,L的电流-电压曲线上移,但不改变其基本形状;②20μmol/L ICA可以使钙通道稳态失活曲线左移并可减慢L-型钙通道失活后的恢复过程。结论:ICA对ICa,L具有浓度依赖性阻滞作用,这可能是其抗心律失常的重要机制之一。     

KCNE2对Kv4.3通道功能的调节作用

目的研究KCNE2对人类心肌细胞瞬间外向钾电流的主要α亚基-Kv4.3功能的调节。方法通过基因转染技术将Kv4.3或Kv4.3与KCNE2cDNA转入COS-7细胞株,采用膜片钳全细胞记录方式记录通道电流。结果KCNE2对Kv4.3功能有明显调控作用:减小Kv4.3通道电流密度;Kv4.3单独表达组通道电流密度为375.13±112.87pA/pF(n=11),KCNE2与Kv4.3共表达组电流密度为152.96±33.71pA/pF(n=16);减慢Kv4.3通道激活和衰减,在 60mV电压刺激下通道激活达峰值的时间由4.82±0.32ms(n=11)延长至20.41±2.13ms(n=16),P<0.05;通道电压依赖性失活发生正向移位,半数失活电压由-53.62±1.24mV(n=8)移至-46.58±1.6mV(n=10);通道从失活中恢复的速度加快,恢复时间常数由193.43±17.98ms缩短137.71±18.29ms,(n=7,P<0.05)。结论KCNE2可能作为人类心肌细胞膜Kv4.3钾离子通道一个重要的辅助亚基-β亚基参与Ito通道功能的调节。     

异丙肾上腺素对犬右心室肌细胞L型钙电流不均一性的影响

目的测定犬右心室三层心肌细胞上参与离子流平衡的内向电流L型钙电流(ICa.L)的特性,并研究其对异丙肾上腺素的反应。方法经酶解分离获得犬右心室外膜下细胞、M细胞和内膜下细胞,应用全细胞膜片钳技术,记录并比较不同部位心肌细胞的ICa.L,分析使用异丙肾上腺素前后电流-电压曲线的差异。结果ICa.L的峰值电流密度(pA/pF)在右心室外膜下细胞、M细胞和内膜下细胞分别为-4.868±1.362(n=20),-3.594±0.544(n=20)和-2.874±0.547(n=20),差异有统计学意义(F=33.493,P<0.05)。使用0.5μmol/L异丙肾上腺素后,右心室外膜下心肌细胞ICa.L的峰值电流密度由-4.832±1.127(n=11)增至-22.348±4.057(P<0.01),M细胞由-3.726±1.051(n=11)增至-17.992±4.159(P<0.01),心内膜下心肌细胞用药前后变化(-2.714±0.879,-2.987±1.012)差异无统计学意义(P>0.05)。结论ICa.L在犬右心室肌的不同细胞(外膜下心肌细胞、M细胞、内膜下心肌细胞)存在不均一性,β-肾上腺能激动剂可以减小右心室外膜下心肌细胞和M细胞动作电位复极1期末离子流的外向转移。     

过氧化氢对大鼠心室肌细胞钠通道电流的影响

目的 研究过氧化氢(H2O2)对单个大鼠心室肌细胞钠通道电流(INa)的影响.方法 用急性酶解法获得单个大鼠心室肌细胞;用标准的全细胞膜片钳技术记录钠通道电流,观察1 mmol/L H2O2引起单个大鼠心室肌细胞INa改变.结果 在1 mmol/L H2O2作用下,大鼠心室肌细胞INa峰值电流密度从(19.95±4.58)pA/pF减少至(15.19±4.15)pA/pF(n=8,P＜0.05),电流-电压曲线上移,翻转电位左移,但对激活电位、峰电位无明显影响;H2O2对INa稳态激活曲线无明显改变,V0 5从(-64.54±0.16)mV左移至(-66.28±0.32)mV(n=8,P＞0.05),对其稳态失活曲线无明显改变,V0 5从(-91.46±0.17)mV左移至(-94.52±0.25)mV(n=8,P＞0.05);H2O2对INa失活后再激活曲线有明显改变,对照组τ为(6.43±1.04)ms,H2O2组τ为(8.31±1.48)ms(n=6,P＜0.05).结论 过氧化氢可以减少大鼠心肌细胞INa,且使其复活明显减慢.     

冬虫夏草对豚鼠心室肌细胞胞浆钙离子浓度及L-型钙电流的影响

目的　研究冬虫夏草 (Codycepssinensis,CS)水提液对豚鼠单个心室肌细胞胞浆内钙离子浓度 ([Ca2 ]i)及L 型钙电流 (ICa L)的影响。方法　酶解法分离豚鼠单个心室肌细胞 ,应用激光扫描共聚焦显微镜联合全细胞膜片钳技术测定豚鼠心室肌细胞 [Ca2 ]i以及ICa L的变化。结果　应用 0 1mg/mL (生药浓度 )冬虫夏草水提液 ,在静息状态下对 [Ca2 ]i 无影响 ;对 6 0mmol/LKCl诱导的胞浆 [Ca2 ]i升高有促进作用 ,峰值荧光强度在 12 0s时由12 0 4 3± 2 38 4增加至 185 5 2± 32 1 0 (n =6 ,P <0 0 5 )。膜片钳研究结果表明 ,冬虫夏草水提液可明显促进ICa L,使ICa L从 (- 15 1± 2 3)pA/ pF增加到 (- 19 7± 3 2 ) pA/pF (刺激电压为 10mV ,n =8,P <0 0 1)。 结论　冬虫夏草水提液促进心肌细胞钙内流 ,是该药治疗缓慢型心律失常的机制之一。     

犬左右心室肌细胞L型钙电流不均一性的研究

目的测定犬左、右心室3层心肌细胞上参与离子流平衡的内向电流L型钙电流(ICa.L)的特性。方法经酶解分离获得犬左、右心室外膜下细胞、M细胞和内膜下细胞,应用全细胞膜片钳技术,记录并比较不同部位心肌细胞的ICa.L,分析电流-电压曲线。结果ICa.L的峰值电流密度(pA/pF)在右心室外膜下细胞、M细胞和内膜下细胞分别为:-4.896±1.907(n=31),-3.406±0.904(n=37)和-2.788±0.756(n=33),心外膜下心肌细胞与M细胞比较,差异有统计学意义(P<0.05);在左心室分别为:-3.824±1.201(n=18),-4.854±1.485(n=20)和-2.988±1.082(n=17),3者之间两两比较,差异有统计学意义(P<0.05)。ICa.L的峰值电流密度在右心室心外膜下心肌细胞大于左心室(P<0.05),而右心室M细胞小于左心室(P<0.01),心内膜下心肌细胞左、右心室之间差异无统计学意义(P>0.05)。结论ICa.L在犬左、右心室肌的不同细胞(外膜下心肌细胞、M细胞、内膜下心肌细胞)存在不均一性,导致右心室跨室壁的电不均一性较左心室明显。     

乳酸左氧氟沙星对豚鼠心肌细胞延迟整流钾电流的影响

目的:观察氟喹诺酮类药物左氧氟沙星(levofloxacin,LVFX)对豚鼠心肌细胞延迟整流钾电流(IK)的影响。方法:采用酶消化的方法分离出单个豚鼠心室肌细胞,利用全细胞膜片钳技术记录不同浓度的LVFX对豚鼠心室肌细胞IK的影响。结果:①SPX和LVFX浓度依赖地抑制IK的脉冲电流和尾电流,但不影响其原有的电压和时间依赖性。②当LVFX作用浓度分别为0.1,1,10,100,1000μM时,在+50 mV去极化电压下,测得IK的脉冲电流较对照组依次减少了(11.81±1.71)%,(14.51±2.12)%,(22.78±3.58)%,(29.59±2.89)%,(38.13±2.44)%;尾电流依次减少了(6.05±251)%,(12.19±1.49)%,(17.75±2.74)%,(30.05±1.49)%,(48.18±3.71)%。结论:LVFX在不同的浓度下对豚鼠心肌细胞的IK有不同程度的抑制。     

Na+/Ca2+交换体电流在兔左心室壁分布的异质性

目的探讨Na+/Ca2+交换体电流(INa+/Ca2+)在左室肌不同部位的分布特征及其与跨壁复极异质性的关系.方法采用全细胞膜片钳技术,分别记录兔左心室肌内膜下、中层及外膜下细胞的动作电位(AP)、INa+/Ca2+及IK.结果中层细胞AP时程明显长于外膜下细胞(P<0.01);在+40 mV时,外向INa+/Ca2+密度在中层细胞明显大于外膜下及内膜下细胞(P分别＜0.01,0.05);在-100 mV时,内向INa+/Ca2+密度在中层细胞明显大于外膜下(P<0.05);在测试电压为+50mV时,中层细胞的IKs尾电流密度明显小于外膜下细胞(P<0.05), 内膜下、中层及外膜下细胞的IKr尾电流密度无明显区别(P>0.05).结论 INa+/Ca2+与IKs在兔左室肌的分布具有异质性,并导致了跨壁复极异质性的形成.     

Effects of Chinese herbs on multiple ion channels in isolated ventricular myocytes

Background Shensong Yangxin (SSYX) is one of the compound recipe of Chinese materia medica. This study was conducted to investigate the effects of SSYX on sodium current (I(Na)), L-type calcium current (I(Ca,L)), transient outward potassium current (I(to)), delayed rectifier current (I(K)), and inward rectifier potassium currents (I(K1)) in isolated ventricular myocytes. Methods Whole cell patch-clamp technique was used to study ion channel currents in enzymatically isolated guinea pig or rat ventricular myocytes. Results SSYX decreased peak I(Na) by (44.84±7.65)% from 27.21±5.35 to 14.88±2.75 pA/pF (n=5, P&lt;0.05). The medicine significantly inhibited the I(Ca,L). At concentrations of 0.25, 0.50, and 1.00 g/100 ml, the peak I(Ca,L) was reduced by (19.22±1.10)%, (44.82±6.50)% and (50.69±5.64)%, respectively (n=5, all P&lt;0.05). SSYX lifted the I-V curve of both I(Na) and I(Ca,L) without changing the threshold, peak and reversal potentials. At the concentration of 0.5%, the drug blocked the transient component of I(to) by 50.60% at membrane voltage of 60 mV and negatively shifted the inactive curve and delayed the recovery from channel inactivation. The tail current density of I(K) was decreased by (30.77±1.11)% (n=5, P&lt;0.05) at membrane voltage of 50 mV after exposure to the medicine and the time-dependent activity of I(K) was also inhibited. Similar to the effect on I(K), the SSYX inhibited I(K1) by 33.10% at the test potential of –100 mV with little effect on reversal potential and the rectification property. Conclusions The experiments revealed that SSYX could block multiple ion channels such as I(Na) I(Ca,L), I(k), I(to) and I(K1), which may change the action potential duration and contribute to some of its antiarrhythmic effects.     

人心肌细胞的分离方法和充血性心力衰竭患者心房肌细胞钾电流的特征

目的：探索人类心房肌细胞的分离方法及充血性心力衰竭（CHF）患者心房肌细胞延迟整流钾电流（Ik）和内向整流钾电流（Ik1）的特征。方法：酶法分离心肌细胞；全细胞膜征钳法记录电流。结果：两种酶学分离方法均能成功地分离出合格的心肌细胞。其中，用I型胶原酶和蛋白酶分离出的活细胞的比例约为40%-50%，而且理想的细胞较多；而用V型胶原酶则仅能分离出1%-3%的活细胞。细胞分离过程受消化酶的类型、季节、病种、心功能等多种因素的影响。以上任一因素发生变化，分离细胞的质和量均会发生改变。利用掌握的全细胞膜片钳技术，我们对人心肌细胞上的钾电流进行了探索。结果显示，在充血性心衰患者心房肌细胞上，存在着Ik和Ik1。其中，Ik的激活较慢，其电流轨迹在刺激开始后缓慢上升，至刺激中止前达到顶点。复极至-30mV时，可引导出Ik的尾电流。与时间依赖性电流相比，此电流的幅值较小。与Ik相比，Ik1的激活较快，激活后迅即趋于稳态，不失活。当膜电位处于不同的电位水平时，Ik1分别表现为内向电流和外向电流，并且随着膜电位的增大，内向电流逐渐减小，外向电流则越来越大。结论：人心肌细胞的分离过程受多种因素的影响。对于CHF患者而言，其心房肌细胞上存在着Ik和Ik1，这两种电流具有不同的电生理特征。     

Effects of Xinjining(心悸宁) Extract on Inward Rectifier Potassium Current in Ventricular Myocytes of Guinea Pig

<正>Objective:To study the effect of Xinjining extract(心悸宁,XJN) on inward rectifier potassium current(I_(K1)) in ventricular myocyte(VMC) of guinea pigs and its anti-arrhythmic mechanism on ion channel level. Methods:Single VMC was enzymatically isolated by zymolisis,and whole-cell patch clamp recording technique was used to record the I_(K1) in VMC irrigated with XJN of different concentrations(1.25,2.50,5.00 g/L;six samples for each).The stable current and conductance of the inward component of I_(K1) as well as the outward component of peak I_(K1) and conductance of it accordingly was recorded when the test voltage was set on -110 mV.Results:The suppressive rate of XJN on the inward component of I_(K1) was 9.54%±5.81%,34.82%±15.03%,and 59.52%±25.58%with a concentration of 1.25,2.50,and 5.00 g/L,respectively,and that for the outward component of peak I_(K1) was 23.94%±7.45%,52.98%±19.62%,and 71.42%±23.01%,respectively(all P0.05).Moreover, different concentrations of XJN also showed effects for reducing I_(K1) conductance.Conclusion:XJN has inhibitory effect on I_(K1) in guinea pig's VMC,and that of the same concentration shows stronger inhibition on outward component than on inward component,which may be one of the mechanisms of its anti-arrhythmic effect.     

1-磷酸鞘氨醇对豚鼠心室肌细胞单通道延迟整流钾电流的影响

目的： 观察1-磷酸鞘氨醇（S1P）对豚鼠心室肌细胞单通道延迟整流钾电流的影响,探讨S1P在室性心律失常中的作用。方法： Langendorff离体心脏逆向灌流法分离豚鼠心室肌细胞,随机选取心室肌细胞分为正常对照组、S1P(2.2 μmol·L^-1)组及S1P(2.2 μmol·L^-1)+Suramin（200 μmol·L^-1）组。应用细胞贴附式记录方式记录心室肌细胞延迟整流钾电流（I_K）。结果：细胞贴附式记录及通道动力学分析 ,S1P组心室肌细胞通道开放时间及开放概率明显低于正常对照组(P<0.05),关闭时间明显高于正常对照组（P<0.05）;S1P+Suramin组通道开放时间、开放概率以及关闭时间与正常对照组比较差异无显著性（P>0.05）。结论： S1P抑制心室肌细胞延迟整流钾电流外流,该作用通过缩短开放时间、延长关闭时间、降低开放概率实现,且通过膜受体介导。     

Effects of Arecoline on Calcium Channel Currents and Caffeine—induced Calcium Release in Isolated Single Ventricular Myocyte of Guinea Pig

Summary The effects of Arecoline (Are) on calcium mobilization were investigated. In isolated single ventricular myocyte of guinea pig, patch clamp whole cell recording techniques were used to record the current of L-type calcium channel and cytosolic Ca²⁺ level (Ca²⁺i) labeled with fluorescence probe Fluo-3/AM was measured under a laser scanning confocal microscope. Results revealed that Are (3–100 μmol/L) could inhibit L-type calcium current in a concentration-dependent manner and the value of IC₅₀ was 33.73 μmol/L (n=5). In the absence of extracellular calcium, the resting levels of [Ca²⁺]i was not affected by Are (n=6,P>0.05), but pretreatment with Are (30 μmol/L) could significantly inhibit the [Ca²⁺]i elevation induced by caffeine (10 mmol/L,n=6,P<0.01). It was concluded that Are could inhibit not only calcium influx through L-type calcium channel but also calcium release from sarcoplasmic reticulum. This project was supported by a grant from Natural Sciences Foundation of China (No. 39670661).     

Na+/Ca2+ exchanger current and K+ current remodeling in midmyocardial cells of hypertrophic left ventricle]

OBJECTIVE: To investigate the characteristics of Na+/Ca2+ exchanger current (INa+ /Ca2+) and K+ current remodeling in midmyocardial cells of hypertrophic left ventricle for understanding the ionic basis of arrhythmia of the hypertrophic heart. METHODS: Twenty New Zealand rabbits were divided equally into normal control group and operation group, and in the latter, left ventricular hypertrophy was induced in the rabbits by partial ligation of the abdominal aorta. Action potentials, INa+/Ca2+, slowly activating delayed rectifier K+ current (IKs) and rapidly activating delayed rectifier K+ current (IKr) were recorded in the two groups by using whole-cell patch-clamp technique. RESULTS: At the basic cycle length of 2 s, 90% action potential duration (APD90) in control and operation groups was 522.0+/-19.5 ms (n=6) and 664.7+/-32.7 ms (n=7) respectively; at the testing potential of +40 mV, outward INa+/Ca2+ density in the two groups was 0.94+/-0.11 pA/pF (n=9) and 1.30+/-0.11 pA/pF (n=8) respectively; the testing potential of -100 mV elicited inward INa+/Ca2+ density of 0.40+/-0.05 pA/pF (n=9) and 0.56+/-0.02 pA/pF (n=8) respectively. The testing potential of +50 mV induced IKs tail current density of 0.26+/-0.03 pA/pF (n=8) and 0.17+/-0.01 pA/pF (n=9), and IKr tail current density of 0.34+/-0.02 pA/pF (n=8) and 0.23+/-0.02 pA/pF (n=9) respectively. Statistically significant differences were identified between the control and operation groups in all the above indices measured. CONCLUSION: The characteristics of electrical remodeling changes in midmyocardial cells of hypertrophic left ventricle, exhibited by prolonged action potential, up-regulated INa+/Ca2+ and down-regulated IKs and IKr.     

D型钠尿肽对豚鼠胃窦环形肌细胞钙敏感钾电流的影响及其作用机制

[目的]记录D型钠尿肽（DNP）对豚鼠胃窦环形肌钙敏感钾电流[IK（Ca）]的影响以探讨DNP抑制胃动力的离子通道机制。[方法]用全细胞式膜片钳技术观察DNP对豚鼠胃窦环形肌细胞IK。、和瞬间外向钾电流（STOCs）的影响。[结果]DNP明显增加豚鼠胃窦环形肌IK‰1和STOCs,并显示剂量依赖关系。0．1、1、10和100nmol/L的DNP能增加IK‰、的幅度,分别为（16．7&#177;1．12）％、（26．5&#177;2．3）％、（46．2&#177;3．3）％和（58．3&#177;3．7）％.细胞外液用无钙液或Rynodine受体的阻断剂均不能阻断此效应,但IP3受体的阻断剂肝素或鸟苷酸环化酶抑制剂LY83583能抑制这种效应。另外,cGMP敏感的磷酸酯酶抑制剂Zaparinast可明显增强DNP对STOCs的增加作用。[结论]DNP通过增加cGMP的产生和激活IP3受体使豚鼠胃窦环形肌细胞上IK（Ca）增加,细胞超极化,从而实现对胃窦环形肌的舒张作用。