A comparison of the actions of cobra cardiotoxin and scorpion toxin II on the guinea-pig taenia coli.

Both cobra cardiotoxin (CTX) and scorpion toxin II induce contracture of the guinea-pig taenia coli, the latter being more potent than the former. Tachyphylaxis was observed with each toxin. Acetylcholine (ACh) contracture was enhanced by toxin II but not by CTX. High K+ (152 mM) abolished toxin II contracture but only partially inhibited CTX and ACh contractures. Ca2+-free medium, especially in the presence of 1 mM EGTA, inhibited CTX- and toxin II-contracture by more than 60%, but abolished ACh contracture. On the other hand, high Ca2+ (12 mM) was without effect on ACh contracture but inhibited both CTX- and toxin II-contracture, and enhanced K+ contracture. Contracture was produced after washout of Ca2+-free medium and toxins but not after washout of high Ca2+ medium, suggesting that the binding of toxins was inhibited by high Ca2+. Tetrodotoxin (TTX) abolished toxin II contracture, but only partially inhibited CTX contracture. Atropine markedly inhibited toxin II contracture but did not significantly affect CTX contracture. Procaine potentiated CTX contracture but abolished toxin II contracture. The spontaneous contraction induced by toxin II was also inhibited by TTX, atropine and procaine. ACh contracture was abolished by atropine and potentiated by procaine, but unaffected by TTX. The rate of decline of K+ (60 mM) contracture in Ca2+-free medium was enhanced by CTX but unaffected by toxin II. 45Ca2+ efflux was increased by CTX more than by toxin II. Both toxins also significantly increased 45Ca2+ uptake. These findings indicate that CTX induces contracture of taenia coli mainly by releasing the Ca2+ pool of the muscle membrane, whereas toxin II does so mainly by releasing acetylcholine from nerve terminals and partially by acting on the muscle membrane as a result of an increase of the membrane Na+ permeability.