Journal of Southern Medical University ›› 2004, Vol. 24 ›› Issue (06): 609-613,618.

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Ionic mechanisms of a novel neurotoxin from the sea anemone Anthopleura sp.in rat ventricular myocytes

OUYANG Ping1, DENG Chun-yu2, LIU Wen-hua3, WANG Lei3, LIANG Dong3, QIAN Wei-min2, XU An-long3   

  1. 1. 第一军医大学南方医院心血管内科, 广东, 广州, 510515;
    2. 广东省人民医院电生理研究室, 广东, 广州, 510080;
    3. 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
  • Online:2004-06-20 Published:2004-06-20

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 μmol/L) myocytes showed no significant difference (P>0.05), but the time constants for inactivation (τh) were significantly greater (P<0.05) for the treated cells over the entire course of the experiment, while the time constants for activation (τm) 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.

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