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.
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine
- Physiology (medical)