Barium-induced automaticity in relation to calcium ions and norepinephrine in the rabbit left atrium.

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 Ba + . The magnitude of the resting potential and of the overshoot decreased with increasing [Ba + ]o, whereas duration of the action potential and rise time increased with increasing [Ba + ]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 [Ca + ]o, threshold concentrations of Ba for inducing automaticity were lower than those at normal [Ca]o. Ba + markedly prolonged the action potential plateau in solutions deprived of Ca . The size of the overshoot was increased and the rise time was shortened despite a significant reduction in the resting potential. Ba partly restored atrial contractility abolished at zero [Ca]o. Each electrical discharge evoked an individual contraction, and a sufficiently fast discharge led to summation of the contractions. Pacemaker activity induced by Ba was suppressed by adding Ca and Mg + . The threshold potential was raised by Ca and Mg + . Threshold concentrations of Ba for inducing automaticity were not influenced by previous treatment with reserpine. It is postulated that Ba 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 Ba serves as a current-carrying ion at zero [Ca]o. It seems unlikely that cardiac norepinephrine participates in pacemaker activity induced by Ba . ADDITIONAL