【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。更多还原

【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 (I Na , I Ca, L and I Na-Ca , respectively) in the isolated single rat ventricular myocytes with or without rhk2a treatment. Results The current-voltage (I-V) relationship for whole-cell I Na in the non-treated and rhk2a-treated (at the dose of 1 μmol/L) myocytes showed no significant difference (P>0.05), but the time constants for inactivation (τ h ) were significantly greater (P<0.05) for the treated cells over the entire course of the experiment, while the time constants for activation (τ m ) exhibited no significant difference between the two cells. The inactivation curve of I Na 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 (I Ca,L ) and I Na-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 I Ca, L or I Na-Ca .更多还原