Delayed afterdepolarizations and triggered activity induced in feline Purkinje fibers by α-adrenergic stimulation in the presence of elevated calcium levels

We studied the ability of α-adrenergic stimulation to induce delayed afterdepolarizations and triggered activity in Purkinje fibers from cat hearts in the presence of an elevated Ca⁺⁺ concentration. Delayed afterdepolarizations could not be induced at drive cycle lengths of 200 to 500 msec in the presence of extracellular Ca⁺⁺ concentrations of 2.7 to 8.1 mM. However, the addition of 10^-5M phenylephrine in the presence of 5 x 10^-7M propranolol elicited delayed afterdepolarizations in eight of 10 preparations at a Ca⁺⁺ concentration of 8.1 mM; nondrive-triggered action potentials were recorded from three of the preparations. These afterpotentials were completely suppressed by 5 x 10^-7M prazosin or 10^-6M phentolamine. In the presence of 5 x 10^-7M propranolol, 10^-5M phenylephrine prolonged action potential duration and this effect was suppressed by 5 x 10^-7M prazosin. Methoxamine, at a concentration of 5 x 10^-6M, was also observed to potentiate delayed afterdepolarizations in all of three preparations studied. These results demonstrate that α-adrenergic stimulation can induce afterpotentials in the presence of elevated Ca⁺⁺ levels in cat hearts. Stimulation of α-adrenoceptors may be responsible for arrhythmias under Ca⁺⁺-loaded conditions such as ischemia and coronary reperfusion.