Huang S J, Kwan C Y
Department of Physiology, Faculty of Medicine, University of Hong Kong, Hong Kong.
Life Sci. 1996;59(4):PL55-60. doi: 10.1016/0024-3205(96)00305-0.
The effects of cardiotoxin (CTX), purified from the venom of Chinese Cobra (Naja naja atra) by a three-step chromatography, on the contractile responses of isolated guinea pig papillary muscle preparation and its antagonism by lanthanum ion (La3+) and divalent cations were examined. CTX induced tonic contraction following a transient augmentation of electrically evoked rhythmic contractions, which is similar to that seen in perfused heart preparation. Multivalent cations, La3+, Ca2+, Mn2+ and Mg2+, concentration-dependently blocked CTX-induced contraction. In Ca(2+)-free medium, CTX did not induce contraction and CTX-induced contraction was not modified in Na(+)-free medium. Nifedipine (1 mumol/L), effectively blocked KCl-induced contracture, but only partially inhibited CTX-induced contraction; thus suggesting that Ca2+ influx induced by CTX utilizes channels other than L-type Ca2+ channels. These cations may compete with CTX for the negatively charged membrane binding site which is responsible for the modulation of Ca2+ movement.
通过三步色谱法从中华眼镜蛇（舟山眼镜蛇）毒液中纯化得到的心脏毒素（CTX），对豚鼠离体乳头肌标本收缩反应的影响及其被镧离子（La3 +）和二价阳离子的拮抗作用进行了研究。CTX在电诱发的节律性收缩短暂增强后诱导强直性收缩，这与在灌注心脏标本中观察到的情况相似。多价阳离子La3 +、Ca2 +、Mn2 +和Mg2 +浓度依赖性地阻断CTX诱导的收缩。在无Ca2 +的培养基中，CTX不诱导收缩，在无Na +的培养基中，CTX诱导的收缩也无变化。硝苯地平（1 μmol/L）有效阻断KCl诱导的挛缩，但仅部分抑制CTX诱导的收缩；因此表明CTX诱导的Ca2 +内流利用的是除L型Ca2 +通道以外的其他通道。这些阳离子可能与CTX竞争负责调节Ca2 +运动的带负电荷的膜结合位点。
