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新型重组海葵毒素hk2a对大鼠心室肌细胞离子通道的影响
引用本文:欧阳平,邓春玉,刘文华,王磊,粱东,钱卫民,徐安龙. 新型重组海葵毒素hk2a对大鼠心室肌细胞离子通道的影响[J]. 南方医科大学学报, 2004, 24(6): 609-613,618
作者姓名:欧阳平  邓春玉  刘文华  王磊  粱东  钱卫民  徐安龙
作者单位:第一军医大学南方医院心血管内科,广东,广州,510515;广东省人民医院电生理研究室,广东,广州,510080;中山大学生命科学学院国家高技术发展计划海洋功能基因组开放实验室,广东,广州,510275
基金项目:This study is supported by State Hi-Tech Development Project of China (2001AA628090),by Guangzhou Sci-tech Committee Foundation (2002Z3-E4131)
摘    要:目的观察新型基因重组海葵毒素rhk2a对大鼠心室肌细胞离子通道的影响。方法采用全细胞膜片钳技术分别记录rhk2a对大鼠心室肌细胞钠电流、L型钙电流和钠-钙交换电流的影响。结果与对照组相比,新型重组海葵毒素rhk2a能够明显减慢大鼠心室肌细胞钠通道的时间依赖性失活(τh)(14.15±4.6 ms vs2.03±0.30 ms, P<0.05),而rhk2a对大鼠心室肌细胞钙通道电流(-8.86±0.35 PA/PF vs-8.99±0.64 PA/PF,P>0.05)和钠-钙交换电流(-0.65±0.2 PA/PF vs-0.69±0.15 PA/PF, P>0.05)无明显直接作用。结论rhk2a对大鼠心室肌细胞钠通道的时间依赖性失活的减慢是rhk2a对心脏具有正性肌力效应的重要机制。

关 键 词:海葵毒素  全细胞膜片钳技术  心肌  钠通道  钙通道  钠钙交换

Ionic mechanisms of a novel neurotoxin from the sea anemone Anthopleura sp.in rat ventricular myocytes
Abstract. Ionic mechanisms of a novel neurotoxin from the sea anemone Anthopleura sp.in rat ventricular myocytes[J]. Journal of Southern Medical University, 2004, 24(6): 609-613,618
Authors:Abstract
Abstract:Objective To determine the ionic mechanisms of a novel neurotoxin rhk2a obtained from the sea anemone Anthopleura sp. in rat ventricular myocytes. Methods Whole-cell patch-clamp recording technique was used to record the sodium, calcium, and sodium-calcium exchange currents (INa, ICa L and INa-Ca respectively) in the isolated single rat ventricular myocytes with or without rhk2a treatment. Results The current-voltage (I-V) relationship for whole-cell INa in the non-treated and rhk2a-treated (at the dose of 1 μ mol/L) myocytes showed no significant difference (P>0.05), but the time constants for inactivation (Th) were significantly greater (P<0.05) for the treated cells over the entire course of the experiment, while the time constants for activation (Tm) exhibited no significant difference between the two cells. The inactivation curve of INa of rhk2a-treated cells was similar to that of the non-treated cells, as with the I-V relationship for whole-cell L-type calcium current (ICa,L) and INa-Ca). Conclusions Delayed inactivation of Na+ channel plays an important role in the positive inotropic effect of rhk2a, possibly resulting from the alteration in Na+ channel kinetics induced by rhk2a. rhk2a does not directly affect Ica,L or INa-Ca.
Keywords:neurotoxins   sea anemone  whole-cell patch-clamp techniques  myocardium  Na channels  Ca 2 channels  sodium-calcium exchange  
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