Palytoxin disrupts cardiac excitation-contraction coupling through interactions with P-type ion pumps.

Palytoxin is a coral toxin that seriously impairs heart function, but its effects on excitation-contraction (E-C) coupling have remained elusive. Therefore, we studied the effects of palytoxin on mechanisms involved in atrial E-C coupling. In field-stimulated cat atrial myocytes, palytoxin caused elevation of diastolic intracellular Ca(2+) concentration ([Ca(2+)](i)), a decrease in [Ca(2+)](i) transient amplitude, Ca(2+) alternans followed by [Ca(2+)](i) waves, and failures of Ca(2+) release.

Dual regulation of cardiac Na+-K+ pumps and CFTR Cl- channels by protein kinases A and C.

Regulation of Na+-K+ pump current (I(p)) and cystic fibrosis transmembrane conductance regulator (CFTR) Cl- current (I(CFTR)) by protein kinases A and C (PKA and PKC) was compared under identical experimental conditions by simultaneous measurement of the two currents in guinea-pig ventricular myocytes whole-cell voltage-clamped at 30-32 degrees C. Membrane current (I) was monitored at a holding potential (V) of -20 mV. I/ V relationships were obtained by hyperpolarizing voltage ramps.