Effects of palytoxin on porcine coronary artery rings

Palytoxin, in concentrations as low as 100 fM, caused contractions of porcine coronary artery rings. Palytoxin concentrations of less than 1 nM caused slowly developing contractions which were not maximal even after 2 h. Rings contracted by 100 nM palytoxin achieved maximal tension by 10 min and relaxed to 53% of that maximum after 2 h. Verapamil (1 microM) reduced the rate of contractions induced by 10 nM palytoxin. Exposure of rings to greater than 10 nM palytoxin for 1-2 h reduced contractions to potassium 18 h later to 61% of the expected contraction and abolished those to palytoxin administered later. Both 10 and 100 nM palytoxin depleted potassium from coronary artery rings. Verapamil (10 microM) prevented potassium depletion by 10 nM palytoxin, but neither 10 microM verapamil nor 1 microM nifedipine prevented potassium depletion in rings exposed to 100 nM palytoxin. Thus, the contractile action and the potassium depleting action of palytoxin on the porcine coronary artery involve mobilization of nifedipine- and verapamil-sensitive calcium. Verapamil- and nifedipine-sensitive calcium was not required for depletion of potassium by the highest PTX concentration (100 nM), however.