Mechanism by which metabolic inhibitors depolarize cultured cardiac cells.

AUTOR(ES)

Clusin, W T

RESUMO

To elucidate the means by which metabolic inhibition depolarizes cardiac cells, spontaneously beating chicken embryonic myocardial cell aggregates were voltage clamped during superfusion with 2,4-dinitrophenol and iodoacetic acid. In aggregates continuously clamped in the pacemaker potential range, abrupt exposure to these metabolic inhibitors produced a slow transient inward current. This inward current was not due to an alteration of the pacemaker current, IK2, because it could still be elicited after IK2 was abolished by Cs+ ions. The inward current was increased by hyperpolarization and decreased by depolarization. It became larger and more sustained if intermittent action potentials were allowed during exposure or if the aggregates were pretreated with either 10 mM Ca2+ or 2.7 microM acetylstrophanthidin. The inward current was suppressed by removal of extracellular Na+ or Ca2+. These observations suggest that early depolarization of cultured cardiac cells by metabolic inhibitors involves some of the same mechanisms as the transient inward current of digitalis toxicity--specifically, an effect of intracellular Ca2+ ions on membrane permeability. Similar phenomena could occur during other forms of metabolic inhibition such as myocardial ischemia.

Documentos Relacionados

• Sodium channels in cultured cardiac cells.
• The mechanism of zinc uptake by cultured rat liver cells.
• Dopamine transporters depolarize neurons by a channel mechanism
• Mechanism by which albumin stimulates renin secretion in isolated kidneys and juxtaglomerular cells.
• Serum and epidermal growth factor transiently depolarize quiescent BSC-1 epithelial cells.