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Effect of valsartan on calcium channel current and sodium-calcium exchanger current in heart failure rats
Authors:DENG Chun-yu  LIN Shu-guang  WU Wei-kang  QIAN Wei-min  RUAN Xiao-wei  WU Shu-lin
Institution:1.Division of Clinical Electrophysiology, Guangdong Cardiovascular Institute, 2Department of Pathophysiology, Basic Medicine Institute, Sun Yat-sen University, Guangzhou 510080, China
Abstract:AIM: To determine the effects of valsartan on calcium channel and sodium-calcium exchanger current in isolated ventricular myocytes of congestive heart failure (CHF) rats. METHODS: Eight weeks after coronary ligation, the rats with heart failure were confirmed by measuring the hemodynamic parameters and divided randomly into the group treating with valsartan (CHF-T, 20 mg/kg) and placebo (CHF-C). Sham-operated group rats served as negative controls (PS). Twelve weeks later, 6 rats were selected randomly for the study of ion channel. Single ventricular myocytes of rats were isolated by enzymatic dissociation. The whole-cell patch-clamp recording technique was used to record calcium channel current and sodium-calcium exchanger current. RESULTS: (1) In the hemodynamic variables, HR and blood pressure were not significantly different in three groups. Compared CHF-C with PS group, LVEDP and Cm increased, LVSP and ±dp/dtmax decreased (P<005). Compared CHF-T group with CHF-C group, LVEDP and Cm decreased, LVSP and ±dp/dtmax increased (P<005). (2) Calcium channel current in CHF-C decreased significantly (P<005). Calcium channel current in CHF-T group was larger significantly than that in CHF-C group (P<005). (3) The activation, inactivation and recovery curves were not altered in 3 groups (P>005). (4) Na+-Ca2+ exchanger current in CHF-C group increased significantly. Na+-Ca2+ exchanger current in CHF-T group was smaller significantly than that in CHF-C group. However, CHF-T group and PS group were not significantly different. CONCLUSION: Administration of valsartan is effective in preventing from cardiac function deterioration, increases calcium channel current and decreases Na+-Ca2+ exchanger current in ventricular myocytes of heat failure rats.
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