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Cesium Abolishes the Barium‐Induced Pacemaker Potential and Current in Guinea Pig Ventricular Myocytes
Author(s) -
SHEN JIANBING,
VASSALLE MARIO
Publication year - 1994
Publication title -
journal of cardiovascular electrophysiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.193
H-Index - 138
eISSN - 1540-8167
pISSN - 1045-3873
DOI - 10.1111/j.1540-8167.1994.tb01145.x
Subject(s) - depolarization , barium , voltage clamp , diastolic depolarization , biophysics , conductance , resting potential , membrane potential , medicine , myocyte , electrophysiology , chemistry , sinoatrial node , biology , physics , heart rate , blood pressure , inorganic chemistry , condensed matter physics
Cesium Abolishes Barium‐Induced PM Current. Introduction: The ability of cesium to block barium‐induced diastolic depolarization (“Ba‐DD”) and pacemaker current was tested in isolated ventricular myocytes. Because Ba‐DD is due to decreasing k conductance and there is no I f at the resting potential, this approach permits verification of whether Cs + is a specific blocker of I, or if it instead also blocks a K + pacemaker current. Methods and Results: Guinea pig isolated ventricular myocytes were studied by a discontinuous, single electrode, voltage clamp method. During hyperpolarizing voltage clamp steps from ‐80 up to ‐140 mV in Tyrode's solution, the inward current increased as a function of voltage but did not change us a function of time (no I f or K + depletion). Cesium (4mM) reduced the current size during the hyperpolarizing steps hut did not induce or unmask time‐dependent currents. Barium (0.05 to 0.1 mM) induced diastolic depolarization, and, in its presence, depolarizing voltage clamp steps were followed by an outward tail current that reversed at ‐92.0 ± 1.3 mV. Outward tail currents were larger at ‐50 mV than at the resting potential, and inward tail currents decayed more rapidly and to a larger extent during larger hyperpolarizing steps. In the presence of Ba 2+ , Cs + (4 mM) had little effect on the steady‐state current but markedly reduced or abolished undershoot, Ba‐DD, and time‐dependent tail currents at potentials both positive and negative to the resting potential. Cs + had a smaller effect on the steady‐state current‐voltage (I‐V) relation in the presence than in the absence of Ba 2+ , as part of the I kl channels were already blocked by Ba 2+ and the time‐dependent changes induced by Ba 2+ were not present. Both Ba 2+ and Cs + had little blocking effect on the steady‐state current positive to the negative slope region of the I‐V relation. Conclusion: In ventricular myocytes, Cs + abolishes the Ba 2+ ‐induced pacemaker current by blocking the time‐dependent change in K + conductance, not by blocking I f. Because Cs + can also block a decaying K + pacemaker current, the abolition of a pacemaker current by Cs + in other cardiac tissues cannot be taken as unequivocal proof that the blocked current is I f