Calcium-dependent slow action potentials in potassium-depolarized guinea-pig ventricular myocardium enhanced by barium ions.

Experiments were performed to investigated the mechanism by which Ba ions facilitate slow response in the myocardium. In partially depolarized guinea-pig papillary muscles, adding 0.2 mmol/l Ba to K-rich solution drastically lowered the stimulus threshold and converted the graded response to an all-or-none activity. This change was accompanied by an increase in the membrane resistance, as determined by cable analysis. When [Ca]0 was altered (0.9--7.2 mmol/l) in the presence of 0.2 mmol/l Ba, the action potentials varied almost in a manner expected for a Ca-electrode, and there were concomitant increases in the twitch tension. The electrical and mechanical activities of muscles treated with 1 mmol/l Ba were also strongly Ca-dependent. At normal [Ca]0, increasing [Ba]0 from 0.2--1 mmol/l only slightly enhanced the action potentials without any appreciable change in the peak twitch tension. When [Ca]0 was lowered to 0.2 mmol/l, elevation of [Ba]0 to over 0.5 mmol/l restored the action potentials, and the resting tension increased. These results suggest that the facilitatory action of the low concentration of Ba on the Ca-dependent slow action potentials is due to a reduction in the membrane shunting conductance and not to a development of any sizeable inward Ba current. However, Ba-dependent action potentials may be generated under conditions of Ca-deficiency. Isoprenaline (0.5--5 x 10(-7) mol/l) induced an automatic activity in the Ba-treated muscles and this phenomenon is probably related to both the drug-induced increase in Ca-permeability and the Ba-induced decrease in shunting conductance. Thus Ba ions appear to be a feasible tool for studies on the myocardial slow channel.