Abstract
Atrial muscle fibers of the guinea pig were depolarized and rendered inexcitable by elevation of [K+]o to 22 mM. Isoproterenol, epinephrine, and norepinephrine restored propagated action potentials and contractions to atrial cells without changing the resting potential. The peak value of the intracellularly recorded action potentials varied 28 mv for a 10-fold change in [Ca2+]o. Isoproterenol-induced restoration of action potentials was insensitive to large concentrations of tetrodotoxin (3 x 10-6M) but antagonized by Mn2+ (0.2 mM). These data supported the proposal that the catecholamines restored excitability by increasing membrane conductance to Ca2+. In addition to the catecholamines, the divalent cations Ba2+, Sr2+, and Ca2+ restored action potentials to atrial muscle fibers depolarized by elevated K+. The effectiveness of the divalent ions in allowing action potentials was inversely related to the estimated hydrated ionic radii. Like the action potentials observed in the presence of isoproterenol, those permitted by Ba2+, Sr2+, and Ca2+ were prevented by Mn2+ but insensitive to blockade by tetrodotoxin.