Abstract
We have found that afterpotentials can be induced selectively in hypertrophied myocardium from rats with renal hypertension. Three kinds of afterpotentials were recorded by standard microelectrode techniques: early afterdepolarizations, delayed afterdepolarizations, and early afterdepolarizations. The first two kinds of afterpotentials could give rise to triggered spontaneous activity, whereas the last kind did not. Delayed afterdepolarizations were induced in hypertrophied fibers exposed to Tyrode's solution containing high extracellular calcium ([Ca2+]o = 7.2-12 mM) and early afterdepolarizations occurred in hypertrophied fibers exposed to Tyrode's solution containing tetraethylammonium (TEA = 10-30 mM). Neither of these treatments produced afterpotentials in normal myocardium. We found that delayed afterdepolarizations became larger when the stimulation frequency, number of preceding driven beats, or [Ca2+]o was increased. The coupling interval from the upstroke of the last driven action potential to the peak of the delayed afterdepolarization decreased when the stimulation frequency or number of preceding driven beats increased. Hypertrophied fibers treated with high [Ca2+]o that gave rise to triggered activity showed a characteristic relationship between delayed afterpotential magnitude and drive cycle length. In hypertrophied muscles treated with TEA, triggered activity developed from an early afterdepolarizations but terminated with a delayed afterdepolarization. The occurrence of afterpotentials in hypertrophied, but not in normal myocardium, appears to reflect the development of an important electrophysiological alteration that may predispose hypertrophied fibers to develop arrhythmias.