Electromechanical studies of an Anemonia sulcata toxin in mammalian cardiac muscle.
1. In guinea-pig papillary muscles toxin II isolated from the sea anemone Anemonia sulcata (ATX) enhanced the force of contraction without changing the time-to-peak tension. ATX increased the relaxation time. The positive inotropic effect was accompanied by a prolongation in action potential duration. The action potential amplitude and the resting membrane potential remained essentially unchanged. The velocity of depolarization (dV/dtmax) decreased slightly. The effects werenot modified by pretreatment of the animals with reserpine. 2. In preparations partially depolarized by elevated extracellular potassium (14.7 mM KCl) a concentration of 1 X 10(-8) M ATX was ineffective with respect to increase in force of contraction or delay of repolarization. The effects of 1 X 10(-8) M ATX could be reversed by 5 X 10(-7) M tetrodotoxin. 3. Our results suggest that ATX affects the action potential duration by delaying the inactivation of the fast sodium permeability change which initiates the action potential. It is not clear, however, in which manner this effect is related to the increase in force of contraction.
Electromechanical studies of an Anemonia sulcata toxin in mammalian cardiac muscle. 1. In guinea-pig papillary muscles toxin II isolated from the sea anemone Anemonia sulcata (ATX) enhanced the force of contraction without changing the time-to-peak tension. ATX increased the relaxation time. The positive inotropic effect was accompanied by a prolongation in action potential duration. The action potential amplitude and the resting membrane potential remained essentially unchanged. The velocity of depolarization (dV/dtmax) decreased slightly. The effects werenot modified by pretreatment of the animals with reserpine. 2. In preparations partially depolarized by elevated extracellular potassium (14.7 mM KCl) a concentration of 1 X 10(-8) M ATX was ineffective with respect to increase in force of contraction or delay of repolarization. The effects of 1 X 10(-8) M ATX could be reversed by 5 X 10(-7) M tetrodotoxin. 3. Our results suggest that ATX affects the action potential duration by delaying the inactivation of the fast sodium permeability change which initiates the action potential. It is not clear, however, in which manner this effect is related to the increase in force of contraction.