Electrophysiological studies prove that consistent alterations induced by Ba
++ in the transmembrane potential from cardiac, skeletal and smooth muscles are represented by a reduction in the resting potential and a prolongation of the action potential duration (1-3), which would he considered to correlate intimately to a production of automaticity in quiescent muscles unless driven by other cells or by artificial stimuli. Pacemaker activity induced by Ba
++ in the atrial and ventricular myocardium mimics the normal impulse generation with respect to the responses of the spontaneous rate and of the membrane potential to exogenous adrenaline (2) and to electrical rapid stimulation of intracardiac sympathetic nerve fibers (4). It is generally accepted that adrenaline and noradrenaline increase spontaneity of cardiac muscles in association with alterations in the permeability of membrane to cations (5). However, an earlier report (4) shows that cardiac noradrenaline does not seem to participate in automaticity induced by Ba
++.
Calcium ions are well known to play physiologically important roles in regulating the permeability of membrane which underlies the bioelectrical process in cardiac pacemaker and non-pacemaker fibers (5, 6), in the mechanism responsible for the initiation and regulation of cardiac muscle contraction (7, 8), in the release of the sympathetic transmitter from peripheral nerves when excited (9, 10), and in the adrenoceptive receptor mechanism in cardiac muscles (11, 12). It was suggested that Ba
++ served as a current-carrying ion at zero [Ca
++]
0 upon depolarization of the cardiac membrane, and also acted as a substitute of Ca
++ in restoring atrial contractility (4). It has been shown that Ba
++ restores the release of acetylcholine from the superior cervical ganglion which has been abolished by removal of Ca
++ from the perfusion fluid (13), and stimulates the release of catecholamines from cat s adrenal glands perfused with the fluid containing normal [Ca
++]
0 and deprived of Ca
++ (14).
The present study was undertaken to investigate (a) effects of Ba
++ in concentrations sufficient to produce automaticity in quiescent atrial muscles on the transmembrane potential of S-A nodal pacemaker fibers exposed to the normal and the Ca
++-free solution, in comparison with that of atrial fibers, (b) modification by substitution of Ca
++ with Ba
++ of the positive chronotropic response of the pacemaker fibers to sympathetic nerve stimulation and exogenous noradrenaline, and (c) effects of Ba
++ on atrial contractility which had been abolished by removal of Ca
++ from the bathing solution.
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