Inhibitory Mechanism of Carvedilol on L-type Ca^2＋ Current in Rat Ventricular Myocytes

Objectives The effects of carvedilol on calcium current (ICa) were investigated in isolated adult rat ventricular myocytes. Methods ICa was recorded by using whole-cell patch-clamp recording technique. Results Carvedilol reversibly inhibited ICa in a concentration-dependent manner, carvedilol at 0.1,0.3, 1 and 10μmol/L in the extracellular solution decreased peak ICa by 1.52%, 18.04%, 37.34% and 72.18%,respectively. The steady-state inactivation curve of ICa was shifted to more negative potentials, while the activation curve was not altered. The recovery from inactivation was shifted to right direction, it could not be recovered completely. In addition, Pretreatment of ventricular myocytes with prazosin and propranolol couldn‘t block the carvedilol-induced reduction of ICa.Conclusions Carvedilol inhibits ICa in adult rat ventricular myocytes by mechanisms involving preferential interaction with the inactivated state of calcium channel.     

Effect of allitridi on calcium current in rat ventricular myocytes

Background Allitridi is an active compound that is extracted from the garlic. It has effects of anti-atherosclerosis, anti-arrhythmias and lowering blood pressure. But the controversy about the effect on cardiac contractility still exists. Methods Whole-cell patch clamp recording technique was used to record ICa,Lin single cell isolated rat ventricular myocytes. The nifedipine- sensitive L-type calcium current was recorded in the rat ventricular myocytes. Results Allitridi decreased the calcium channel current in a dose-dependent and voltage-dependent manner in ventricular myocytes of rats. The current-voltage curve was shifted upwards, on which active potential,peak potential and reverse potential showed no significant changes. The inactivation curve was shifted to more negative potential, but the activation curve and recovery curve were not altered. Allitridi had no effect on frequent-dependency of calcium current. Conclusion These results show that allitridi could concentration-dependently decrease calcium channel current in ventricular myocytes of rats.     

The Regulation Effects of β2-AR on INCX in Myocytes from Infarcted Rat Heart

Objectives This study is designed to investigate the regulation effects of β2-adrenergic receptors （AR） on expression of the Na^± - Ca^2 ± exchanger （ INCX） in myocytes from the infarcted rat heart. Methods Twenty-eight adult Wistar rats were randomly divided into four groups ： the control group, the two weeks, four weeks and eight weeks post-myocardial infarction （post-MI） groups, respectively. The chest of rat was opened and a ligature was placed around the left anterior descending coronary artery. Rats in control group were sham-operated without the coronary artery ligation. After the operation, rats were fed for two, four or eight weeks respectively. Myocytes were enzymatically disassociated by Langendorff perfusion. The whole cell-patch clamp recording technique was used to record INCX in specific pipette solution and superfusion according to the specific holding potential and command potential program. Results The INCX in ventricular myocytes from the border zone of infarcted myocardium increased significantly at eight weeks after MI （0. 51 ± 0. 12 pA/pF vs 1.07± 0. 21 pA/pF, P 〈0.05）. β2-AR agonist increased INcx more strongly in myocytes from post- MI heart than in controls. β2-AR antagonist attenuated the rise of INCX, strongly in myocytes from post-MI heart than in controls, whereas β1-AR onist. Conclusion The regulation effects of β2-AR on INCX in myocytes AR had closer relationship with the genesis of malignant arrhythmia afte     

Effects of Simvastatin on Ion Channel Currents in Ventricular Myocytes from Acute Infarcted Heart of Normocholesterolemic Rabbits

Objectives To investigate the effects of simvastatin on membrane ionic currents in left ventricular myocytes of rabbit heart suffering from acute myocardial infarction （ AMI）, so as to explore the ionic mechanism of statin treatment for antiarrhythmia. Methods Forty-five New Zealand rabbits were randomly divided into three groups： AMI group, simvastatin intervention group （ Statin group） and sham-operated control group （CON）. Rabbits were infarcted by ligation of the left anterior descending coronary artery after administration of oral simvastatin 5 mg · kg^-1·d^-1 （Statin group） or placebo （AMI group） for 3 days. Single ventricular myocytes were isolated enzymatically from the epicardial zone of the infracted region 72 h later. Whole cell patch clamp technique was used to record membrane ionic currents, including sodium current （INa）, L-type calcium current （Ica-L） and transient outward potassium current （Ito）. Results （1） There was not significant difference in serum cholesterol concentration among three groups. （2） The peak INa current density （at -30 mV） was significantly decreased in AMI group （ -25.26±5.28, n = 13 ）, comparing with CON （ - 42. 78± 5.48, n = 16）, P 〈 0. 05, while it was significantly increased in Statin group （ - 39.83 ±5.65 pA/pF, n = 12） comparing with AMI group, P 〈0. 01 ; The peak Ica-L current density （ at 0 mV） was significantly decreased in AMI group （ -3. 43 ±0. 92 pA/pF, n = 13） comparing with CON （ -4. 56 ±1.01 pA/pF, n = 15）, P 〈0. 05, while it was significantly increased in Statin group （ -4. 18±0. 96 pA/pF, n = 12） comparing with AMI group, P 〈0. 05; The Ito current density （ at ＋ 60 mV） was significantly decreased in AMI group （ 11.41 ± 1.94 pA/pF, n = 13 ） comparing with CON （17.41 ±3.13 pA/pF, n = 15）, P 〈0. 01, while it was significantly increased in Statin group （16. 11 ± 2. 43 pA/pF, n = 14） comparing with AMI group, P 〈 0. 01. Conclusions AMI induces signific     

The ionic mechanisms of long QT interval in diabetic rabbits

Objective Abnormal QT prolongation associated with arrhythmias is considered the major cardiac electrical disorder and a significant predictor of mortality in diabetic patients. The precise ionic mechanisms for diabetic QT prolongation remained unclear. The present study was designed to analyze the changes of ventricular repolarization and the underlying ionic mechanisms in diabetic rabbit hearts. Methods Diabetes was induced by a single injection ofalloxan （145mg/kg, Lv. ）. After the development of diabetes （10 weeks）, ECG was measured. Whole-cell patch-clamp technique was applied to record the action potential duration （APD50, APD90）, slowly activating outward rectifying potassium current （IKs）, L-type calcium current （ICa-L） and inward rectifying potassium current （IK1）. Results The action potential duration （APD50 and APD90） of ventricular myocytes was obviously prolonged from 271.5＋32.3 ms and 347.8＋36.3 ms to 556.6~72.5 ms and 647.9~72.2 ms respectively （P〈 0.05）. Meanwhile the normalized peak current densities of IKs in ventricular myocytes investigated by whole-cell patch clamp was smaller in diabetic rabbits than that in control group at test potential of＋50mV （1.27~0.20 pA/pF vs 3.08~0.67 pA/pF, P〈0.05）. And the density of the ICa-L was increased apparently at the test potential of 10 mV （-2.67~0.41 pA/pF vs -5.404-1.08 pA/pF, P〈0.05）. Conclusion Ventricular repolarization was prolonged in diabetic rabbits, it may be partly due to the increased L-type calcium current and reduced slow delayed rectifier K＋ current （IKs） （J Geriatr Cardio12010; 7：25-29）.     

硫化氢对离体大鼠心室肌细胞ATP依赖的钾通道外向电流的影响

Objective To investigate the effects of endogenous and exogenous hydrogen sulfide (H2S) on the KATP current in isolated rat ventricular myoeytes. Methods Ventrieular myoeytes were isolated from rat heart by modified Langendoff perfusion with collagenase. KATP current of single rat ventricular myocytes was recorded by whole-cell patch-clamp technique. Results The density of KATP current was significantly reduced by 200 μmol/L DL-propargylglyeine (PPG, an irreversible inhibitor of the H2S) [(5.3258±0.7556) pA/pF vs. (3.7856±0.4312) pA/pF, P ＜ 0.01] in a time-dependent way. The density of KATP current could be significantly increased by NariS(a H2S donor, 9.375, 18.75, 37.5,75, 150 μmol/L) in a concentration-dependent manner [(6.6310±0.6092) pA/pF vs. (9.0949±1.0259)pA/pF at 150 μmol/L, P ＜ 0.01]. Conclusion Both endogenous and exogenous H2S could open KATP channels and enhance the KATP current in rat ventricular myocytes.     

硫化氢对离体大鼠心室肌细胞ATP依赖的钾通道外向电流的影响

Objective To investigate the effects of endogenous and exogenous hydrogen sulfide (H2S) on the KATP current in isolated rat ventricular myoeytes. Methods Ventrieular myoeytes were isolated from rat heart by modified Langendoff perfusion with collagenase. KATP current of single rat ventricular myocytes was recorded by whole-cell patch-clamp technique. Results The density of KATP current was significantly reduced by 200 μmol/L DL-propargylglyeine (PPG, an irreversible inhibitor of the H2S) [(5.3258±0.7556) pA/pF vs. (3.7856±0.4312) pA/pF, P ＜ 0.01] in a time-dependent way. The density of KATP current could be significantly increased by NariS(a H2S donor, 9.375, 18.75, 37.5,75, 150 μmol/L) in a concentration-dependent manner [(6.6310±0.6092) pA/pF vs. (9.0949±1.0259)pA/pF at 150 μmol/L, P ＜ 0.01]. Conclusion Both endogenous and exogenous H2S could open KATP channels and enhance the KATP current in rat ventricular myocytes.     

硫化氢对离体大鼠心室肌细胞ATP依赖的钾通道外向电流的影响

Objective To investigate the effects of endogenous and exogenous hydrogen sulfide (H2S) on the KATP current in isolated rat ventricular myoeytes. Methods Ventrieular myoeytes were isolated from rat heart by modified Langendoff perfusion with collagenase. KATP current of single rat ventricular myocytes was recorded by whole-cell patch-clamp technique. Results The density of KATP current was significantly reduced by 200 μmol/L DL-propargylglyeine (PPG, an irreversible inhibitor of the H2S) [(5.3258±0.7556) pA/pF vs. (3.7856±0.4312) pA/pF, P ＜ 0.01] in a time-dependent way. The density of KATP current could be significantly increased by NariS(a H2S donor, 9.375, 18.75, 37.5,75, 150 μmol/L) in a concentration-dependent manner [(6.6310±0.6092) pA/pF vs. (9.0949±1.0259)pA/pF at 150 μmol/L, P ＜ 0.01]. Conclusion Both endogenous and exogenous H2S could open KATP channels and enhance the KATP current in rat ventricular myocytes.     

硫化氢对离体大鼠心室肌细胞ATP依赖的钾通道外向电流的影响

Objective To investigate the effects of endogenous and exogenous hydrogen sulfide (H2S) on the KATP current in isolated rat ventricular myoeytes. Methods Ventrieular myoeytes were isolated from rat heart by modified Langendoff perfusion with collagenase. KATP current of single rat ventricular myocytes was recorded by whole-cell patch-clamp technique. Results The density of KATP current was significantly reduced by 200 μmol/L DL-propargylglyeine (PPG, an irreversible inhibitor of the H2S) [(5.3258±0.7556) pA/pF vs. (3.7856±0.4312) pA/pF, P ＜ 0.01] in a time-dependent way. The density of KATP current could be significantly increased by NariS(a H2S donor, 9.375, 18.75, 37.5,75, 150 μmol/L) in a concentration-dependent manner [(6.6310±0.6092) pA/pF vs. (9.0949±1.0259)pA/pF at 150 μmol/L, P ＜ 0.01]. Conclusion Both endogenous and exogenous H2S could open KATP channels and enhance the KATP current in rat ventricular myocytes.     

硫化氢对离体大鼠心室肌细胞ATP依赖的钾通道外向电流的影响

Objective To investigate the effects of endogenous and exogenous hydrogen sulfide (H2S) on the KATP current in isolated rat ventricular myoeytes. Methods Ventrieular myoeytes were isolated from rat heart by modified Langendoff perfusion with collagenase. KATP current of single rat ventricular myocytes was recorded by whole-cell patch-clamp technique. Results The density of KATP current was significantly reduced by 200 μmol/L DL-propargylglyeine (PPG, an irreversible inhibitor of the H2S) [(5.3258±0.7556) pA/pF vs. (3.7856±0.4312) pA/pF, P ＜ 0.01] in a time-dependent way. The density of KATP current could be significantly increased by NariS(a H2S donor, 9.375, 18.75, 37.5,75, 150 μmol/L) in a concentration-dependent manner [(6.6310±0.6092) pA/pF vs. (9.0949±1.0259)pA/pF at 150 μmol/L, P ＜ 0.01]. Conclusion Both endogenous and exogenous H2S could open KATP channels and enhance the KATP current in rat ventricular myocytes.     

硫化氢对离体大鼠心室肌细胞ATP依赖的钾通道外向电流的影响

Objective To investigate the effects of endogenous and exogenous hydrogen sulfide (H2S) on the KATP current in isolated rat ventricular myoeytes. Methods Ventrieular myoeytes were isolated from rat heart by modified Langendoff perfusion with collagenase. KATP current of single rat ventricular myocytes was recorded by whole-cell patch-clamp technique. Results The density of KATP current was significantly reduced by 200 μmol/L DL-propargylglyeine (PPG, an irreversible inhibitor of the H2S) [(5.3258±0.7556) pA/pF vs. (3.7856±0.4312) pA/pF, P ＜ 0.01] in a time-dependent way. The density of KATP current could be significantly increased by NariS(a H2S donor, 9.375, 18.75, 37.5,75, 150 μmol/L) in a concentration-dependent manner [(6.6310±0.6092) pA/pF vs. (9.0949±1.0259)pA/pF at 150 μmol/L, P ＜ 0.01]. Conclusion Both endogenous and exogenous H2S could open KATP channels and enhance the KATP current in rat ventricular myocytes.     

硫化氢对离体大鼠心室肌细胞ATP依赖的钾通道外向电流的影响

Objective To investigate the effects of endogenous and exogenous hydrogen sulfide (H2S) on the KATP current in isolated rat ventricular myoeytes. Methods Ventrieular myoeytes were isolated from rat heart by modified Langendoff perfusion with collagenase. KATP current of single rat ventricular myocytes was recorded by whole-cell patch-clamp technique. Results The density of KATP current was significantly reduced by 200 μmol/L DL-propargylglyeine (PPG, an irreversible inhibitor of the H2S) [(5.3258±0.7556) pA/pF vs. (3.7856±0.4312) pA/pF, P ＜ 0.01] in a time-dependent way. The density of KATP current could be significantly increased by NariS(a H2S donor, 9.375, 18.75, 37.5,75, 150 μmol/L) in a concentration-dependent manner [(6.6310±0.6092) pA/pF vs. (9.0949±1.0259)pA/pF at 150 μmol/L, P ＜ 0.01]. Conclusion Both endogenous and exogenous H2S could open KATP channels and enhance the KATP current in rat ventricular myocytes.     

硫化氢对离体大鼠心室肌细胞ATP依赖的钾通道外向电流的影响

Objective To investigate the effects of endogenous and exogenous hydrogen sulfide (H2S) on the KATP current in isolated rat ventricular myoeytes. Methods Ventrieular myoeytes were isolated from rat heart by modified Langendoff perfusion with collagenase. KATP current of single rat ventricular myocytes was recorded by whole-cell patch-clamp technique. Results The density of KATP current was significantly reduced by 200 μmol/L DL-propargylglyeine (PPG, an irreversible inhibitor of the H2S) [(5.3258±0.7556) pA/pF vs. (3.7856±0.4312) pA/pF, P ＜ 0.01] in a time-dependent way. The density of KATP current could be significantly increased by NariS(a H2S donor, 9.375, 18.75, 37.5,75, 150 μmol/L) in a concentration-dependent manner [(6.6310±0.6092) pA/pF vs. (9.0949±1.0259)pA/pF at 150 μmol/L, P ＜ 0.01]. Conclusion Both endogenous and exogenous H2S could open KATP channels and enhance the KATP current in rat ventricular myocytes.     

硫化氢对离体大鼠心室肌细胞ATP依赖的钾通道外向电流的影响

Objective To investigate the effects of endogenous and exogenous hydrogen sulfide (H2S) on the KATP current in isolated rat ventricular myoeytes. Methods Ventrieular myoeytes were isolated from rat heart by modified Langendoff perfusion with collagenase. KATP current of single rat ventricular myocytes was recorded by whole-cell patch-clamp technique. Results The density of KATP current was significantly reduced by 200 μmol/L DL-propargylglyeine (PPG, an irreversible inhibitor of the H2S) [(5.3258±0.7556) pA/pF vs. (3.7856±0.4312) pA/pF, P ＜ 0.01] in a time-dependent way. The density of KATP current could be significantly increased by NariS(a H2S donor, 9.375, 18.75, 37.5,75, 150 μmol/L) in a concentration-dependent manner [(6.6310±0.6092) pA/pF vs. (9.0949±1.0259)pA/pF at 150 μmol/L, P ＜ 0.01]. Conclusion Both endogenous and exogenous H2S could open KATP channels and enhance the KATP current in rat ventricular myocytes.     

硫化氢对离体大鼠心室肌细胞ATP依赖的钾通道外向电流的影响

Objective To investigate the effects of endogenous and exogenous hydrogen sulfide (H2S) on the KATP current in isolated rat ventricular myoeytes. Methods Ventrieular myoeytes were isolated from rat heart by modified Langendoff perfusion with collagenase. KATP current of single rat ventricular myocytes was recorded by whole-cell patch-clamp technique. Results The density of KATP current was significantly reduced by 200 μmol/L DL-propargylglyeine (PPG, an irreversible inhibitor of the H2S) [(5.3258±0.7556) pA/pF vs. (3.7856±0.4312) pA/pF, P ＜ 0.01] in a time-dependent way. The density of KATP current could be significantly increased by NariS(a H2S donor, 9.375, 18.75, 37.5,75, 150 μmol/L) in a concentration-dependent manner [(6.6310±0.6092) pA/pF vs. (9.0949±1.0259)pA/pF at 150 μmol/L, P ＜ 0.01]. Conclusion Both endogenous and exogenous H2S could open KATP channels and enhance the KATP current in rat ventricular myocytes.     

Effects of simvastatin on Ion Channel Currents in ventricular myocytes from rabbit with acute myocardial infarction

Objective To investigate the effects of simvastatin on membrane ionic currents in left ventricular myocytes of rabbit heart suffering from acute myocardial infarction(AMI),so as to explore the ionic mechanism of statin treatment for antiarrhythmia. Methods Fourty-five New Zeland rabbits were randomly divided into three groups: AMI group, simvastatin intervention group (Statin group) and sham-operated control group (CON). Rabbits were infarcted by ligation of the left anterior descending coronary artery after administration of oral simvastatin 5 mg?kg-1?d-1 (Statin group) or placebo (AMI group) for 3 days. 24 h later, single ventricular myocytes were isolated enzymatically from the epicardial zone of the infracted region .Whole cell patch clamp technique was used to record membrane ionic currents, including sodium current (INa), L-type calcium current (ICa-L) and transient outward potassium current (Ito). Results There was not significant difference in serum cholesterol concentration among three groups. The peak INa current density(at –30 mV) was significantly decreased in AMI group (–23.26±5.18,n=12),) ompared with CON (–42.78±5.48 , n=16), P<0.05,while it was significantly increased in Statin group (–39.23±5.45 pA/pF, n=13) compared with AMI group, P<0.01;The peak ICa-L current density (at 0 mV) was significantly decreased in AMI group (–3.23±0.91 pA/pF, n=12) compared with CON (–4.56±1.01 pA/pF,n= 15),P<0.05,while it was significantly increased in Statin group (–4.18±0.95 pA/pF, n= 12) compared with AMI group, P<0.05; The Ito current density(at +60 mV) was significantly decreased in AMI group (10.41 ±1.93 pA/pF, n=12) compared with CON (17.41± 3.13 pA/pF , n=15), P<0.01, while it was significantly increased in Statin group (16.21 ± 2.42 pA/pF , n=13) compared with AMI group, P<0.01. Conclusions AMI induces significant down-regulation of INa, ICa-L and Ito pretreatment with simvastatin could attenuate this change without lowering the serum cholesterol level, suggesting that simvastatin could reverse this electrical remodeling, thus contributing to the ionic mechanism of statin treatment for antiarrhythmia .     

Research on Electrical Remodeling After Short Term Pacing in Canine Model

Objectives To evaluate the changes in atrial effective refractory period （AERP） proprieties and in ionic currents in PVs myocytes from dogs subjected to rapid atrial pacing in PVs and right atrial appendage （RAA） and to relate these changes to the ability to induce AF. Methods Twelve mongrel dogs in normal sinus rhythm were paced from the superior left PVs or RAA at 500 bpm for 4 hours. Electrophysiologic studies conducted to determine changes in AERP, dispersion and rhythm. Ionic currents were studies with the patch clamp technique in single PVs myocytes in sham operated dogs and compared with those from PVs pacing and RAA pacing groups. Results The presence of rapid atrial pacing was associated with a marked shortening in AERP in both PVs and RAA pacing group with a marked increase of AERP dispersion in PVs pacing. Both L-type calcium current （Ica L ） and the transient outward current （ Ito ） were reduced in both groups with an increased significance in PVs pacing group. The density of ICa-L was decreased significantly from （ - 6. 03 ± 0. 63 ） pA./pF in the control group to （ -3.21 ±0. 34） pA/pF in PVs pacing group and （ - 4. 75 ± 0. 41 ） pA./pF in RAA pacing group （ n = 6, P 〈 0. 05 ） while the density of Ito was decreased significantly from （8.45 ± 0. 71 ） pA./pF in the control group to （ 5.21 ± 0. 763 ） pA./pF in PVs pacing group and （6. 84 ±0. 69 ） pA./pF in RAA pacing group （ n = 6, P 〈 0. 05 ）. Conclusions Our findings provide likely ionic mechanisms of shortened repolarization in induced atrial tachycardia with a decrease in Ica L and /tocurrent densities which is the likely mechanism for a decrease in Action potential duration （APD） rate adaptation in the canine rapid pacing model more pronounced in PVs pacing group underlying the crucial role of PVs in initiating AF.     

二十二碳六烯酸对大鼠心室肌细胞动作电位和钠通道的影响

Objective To investigate the effects of docosahexaenoic acid (DHA) on action potentials (AP) and sodium channel current(INa) in rat ventricular myocytes. And evaluate the anti-arrhythmia mechanisms of DHA. Methods AP and INa of individual ventricular myocytes were recorded by patch-clamp technique in whole-cell configuration. Effects of DHA on AP and sodium channels were observed when it was applied at 0,20,40,60,80,100,120 μmol/L respectively. Results ( 1 ) APD25, APD50 and APD90 are gradually prolonged with augmentation of DHA(P ＜0. 05 ,n =20). Effects of DHA on AP maximal velocity(vmax) ,AP amplitude ( APA ) and AP overshoot (OS) were not significant difference ( P ＞ 0. 05, n= 20 ). (2) INa were gradually blocked,I-U curves were upward,stably inactivated curves were shifted to the left,and recovered time from inactivation was prolonged, and stably activated curves were no remarkable significance. INa was blocked to 1.51% ±1.32% ,21.13% ±4.62% ,51.61% ±5. 73% ,67. 62% ±6.52% ,73.49% ±7.59% and 79.95%± 7. 62% under manding potential equal to - 30 mV( P ＜ 0. 05,n = 20), and half-effect concentration ( EC50 )of DHA was(47. 91 ± 1.57) μmol/L. Conclusion The effects of DHA on APD and INa may be one of the antiarrhythmia mechanisms of DHA.     

In Vitro Study on Mesenchymal Stem Cells： Anti-apoptotic Effects on Cardiac Myocytes

Objectives To investigate the anti-apoptotic effects of mesenchymal stem cells （MSCs） on hypoxic injured cardiac myocytes in vitro. Methods MSCs were isolated from bone marrow of Sprague-Dawley （SD） rats, and cardiac myocytes from neonatal rats. The rat cardiac myocytes were co-cultured with MSCs or MSC-conditioned media in anoxia （95% N2 ±5% CO2） for 72 hours. Cell apoptosis was measured by Hoechst 33258 staining. The expression of Bcl-2 and Bax in cardiac myocytes was tested by Western Blot. Results The apoptotic rate was 51.6% ± 2.4% when cardiac myocytes were cultured in continuous hypoxia and was significantly decreased when cardiac myocytes were cocultured with MSCs or MSC-conditioned media （ 15.1% ± 5.4% and 24. 0% ± 4.2% respectively, P 〈 0. 001 ）. The decreased expression of Bax in the cardiac myocytes was greatly related to the decreasing of apoptosis, but there was no difference in Bcl-2 expression among these groups. Conclusions Co-cultured MSCs showed significant anti-apoptotic effects on cardiac myocytes in continuous hypoxia. The mechanism may be the interact of cell to cell and paracrine of cytokines which effected the expression of Bax in the cardiac myocytes.     

Effects of tetrandrine on calcium and potassium currents in isolated rat hepatocytes

AIM: To study the effects of tetrandrine (Tet) on calciumrelease-activated calcium current (ICRAC), delayed rectifierpotassium current (IK), and inward rectifier potassiumcurrents (IK1) in isolated rat hepatocytes.METHODS: Hepatocytes of rat were isolated by usingperfusion method. Whole cell patch-clamp techniques wereused in our experiment.RESULTS: The peak amplitude.of ICRAC was -508±115 pA(n＝15), its reversal potential of ICRAC was about 0 mV. At thepotential of -100 mV, Tet inhibited the peak amplitude ofICRAC from -521±95 pA to -338±85 pA (P＜0.01 vs control,n＝5), with the inhibitory rate of 35 % at 10 μmol/L andfrom -504±87 pA to -247±82 pA (P＜0.01 vscontrol, n＝5),with the inhibitory rate of 49 % at 100 μmol/L, withoutaffecting its reversal potential. The amplitude of ICRAC wasdependent on extracellular Ca2+ concentration. The peakamplitude of ICRAC was -205±105 pA (n＝3) in tyrode's solutionwith Ca2+ 1.8 mmol/L (P＜0.01 vs the peak amplitude ofICRAC in external solution with Ca2+ 10 mmol/L). Tet at theconcentration of 10 and 100 μmol/L did not markedly changethe peak amplitude of delayed rectifier potassium currentand inward rectifier potassium current (P＞0.05 vs control).CONCLUSION: Tet protects hepatocytes by inhibiting ICRAC,which is not related to I K and IK1.