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Oscillatory afterpotentials in cardiac tissues are believed to result from an activation of calcium-operated cation channels of mixed selectivity (sodium, potassium), or perturbation of an electrogenic sodium-calcium exchange carrier, by an oscillatory release of calcium from sarcoplasmic reticulum. In the present experiments, the presence and properties of ouabain-induced oscillatory afterpotentials were examined in young (3-day-old) embryonic chick hearts, both fresh and organ cultured for 6-14 days. The hearts did not differentiate in organ culture, and the cells retained slowly rising spontaneous action potentials. To induce the oscillatory afterpotentials, automaticity was suppressed by elevating extracellular K+ ion concentration from 4 mM to 6 mM, and the preparations were electrically stimulated at a rate of 0.5 Hz. Stable oscillatory afterpotentials were induced with 1.3-7.5 microM ouabain. The oscillatory afterpotential amplitude was increased when the stimulation rate was increased to 3 and 4 Hz. The oscillatory afterpotentials were potentiated when extracellular Ca++ ion concentration was increased to 3.6 mM or by the addition of barium (0.1 mM). Low extracellular Na+ ion concentration (40-121 mM), strontium (4 mM), magnesium (2-4 mM), and manganese (1-4 mM) significantly depressed the oscillatory afterpotentials. These properties of the oscillatory afterpotentials are similar to those described for adult mammalian ventricular muscles and Purkinje fibers. Our results suggest that young embryonic chick hearts (which lack fast sodium channels and, instead, have slow sodium channels) possess the calcium-operated mixed cation channels at a very early developmental stage if the oscillatory afterpotentials result from the activation of the mixed cation channels by intracellular calcium.

Properties of oscillatory afterpotentials in young embryonic chick hearts.