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Abstract-Effectsof Goniopora toxin (GPT) on cardiac action potential and on contractile force were investigated in isolated guinea-pig papillary muscle.GPT produced a positive inotropic effect by increasing con tractile force and prolonging the relaxation time. The time-to-peak force was little affected.GPT prolonged the action potential duration but did not affect the resting membrane potential nor the amplitude of the action potential.Thus there was a correlation between the positive inotropic effect and prolongation of the action potential duration. Tetrodotoxin or a reduction in extracellular sodium concentration attenuated both the positive inotropic effect and the prolonged duration of the action potential induced by GPT. Lanthanum or a reduction in extracellular calcium concentration also inhibited the increased contraction but did not shorten the prolonged durations of contraction and action potential. Verapamil attenuated the positive inotropic effect by reducing both the contractile force and the duration of contraction, but did not shorten the action potential duration.These results show that the positive inotropic effect of GPT depends on the increase in both sodium and calcium influxes while the prolonging effect on the action potential probably depends only on an increase in sodium influx. Hence, it is concluded that the prolongation of the action potential due to the increased sodium permeability is an essential process for the appearance of the positive inotropic effect of GPT.

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Effects of a marine polypeptide, Goniopora toxin (GPT) (molecular weight 12,000), were examined in isolated blood vessels guinea pigs. GPT, ranging from 10-100 nM, augmented the contractile response to electrical transmural stimulation in the thoracic aorta, portal vein, and mesenteric and femoral arteries. The effects were abolished by tetrodotoxin and bretylium, and were markedly attenuated by phentolamine. As GTP did not affect the resting tension spontaneous rhythmicity or noradrenaline-induced contraction, the toxin appears to act on the neural elements in the vascular wall rather than on the smooth muscle. In the portal vein preloaded with 3H-noradrenaline, GPT enhanced the 3H-efflux in response to electrical transmural stimulation, yet had not effect on the spontaneous efflux. The increase in stimulation-evoked 3H-efflux caused by GPT was more than 15 times larger than the increase seen with cocaine or phentolamine. Tetrodotoxin completely blocked the 3H-efflux induced by electrical transmural stimulation. These data suggest that GPT acts on nerve components in guinea pig blood vessels and increases the release of noradrenaline evoked by electrical stimulation of the nerve fibers. These effects are probably associated with prolongation of the action potential duration and repetitive discharges in the adrenergic nerve fibers.

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