Barium-Induced Automaticity in Relation to Calcium Ions and Norepinephrine in the Rabbit Left Atrium

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Abstract
Membrane potentials were recorded from a region of the left atrium close to the interatrial septum and from an atrial appendage. Pacemaker activity was induced after exposure to Ba2+. The magnitude of the resting potential and of the overshoot decreased with increasing [Ba2+]o, whereas duration of the action potential and rise time increased with increasing [Ba2+]o. Electrical stimulation for 5 sec at 1/sec to left atria showing automaticity produced bradycardia followed by tachycardia. Bradycardia was abolished by atropine; tachycardia was suppressed by propranolol and previous treatment with reserpine. At zero [Ca2+]o, threshold concentrations of Ba2+ for inducing automaticity were lower than those at normal [Ca2+]o. Ba2+ markedly prolonged the action potential plateau in solutions deprived of Ca2+. The size of the overshoot was increased and the rise time was shortened despite a significant reduction in the resting potential. Ba2+ partly restored atrial contractility abolished at zero [Ca2+]o. Each electrical discharge evoked an individual contraction, and a sufficiently fast discharge led to summation of the contractions. Pacemaker activity induced by Ba2+ was suppressed by adding Ca2+ and Mg2+. The threshold potential was raised by Ca2+ and Mg2+. Threshold concentrations of Ba2+ for inducing automaticity were not influenced by previous treatment with reserpine. It is postulated that Ba2+ antagonizes the movement of K+ across the membrane, resulting in a decrease in the resting potential and a prolongation of the action potential duration, and that Ba2+ serves as a current-carrying ion at zero [Ca2+]o. It seems unlikely that cardiac norepinephrine participates in pacemaker activity induced by Ba2+.