RESUMO
The mechanisms of the hyperpolarizing and depolarizing actions of cesium were studied in cardiac Purkinje fibers perfused in vitro by means of a microelectrode technique under conditions that modify either the Na(+)-K(+) pump activity or I(f). Cs(+) (2 mM) inconsistently increased and then decreased the maximum diastolic potential (MDP); and markedly decreased diastolic depolarization (DD). Increase and decrease in MDP persisted in fibers driven at fast rate (no diastolic interval and no activation of I(f)). In quiescent fibers, Cs(+) caused a transient hyperpolarization during which elicited action potentials were followed by a markedly decreased undershoot and a much reduced DD. In fibers depolarized at the plateau in zero [K(+)](o) (no I(f)), Cs(+) induced a persistent hyperpolarization. In 2 mM [K(+)](o), Cs(+) reduced the undershoot and suppressed spontaneous activity by hyperpolarizing and thus preventing the attainment of the threshold. In 7 mM [K(+)](o), DD and undershoot were smaller and Cs(+) reduced them. In 7 and 10 mM [K(+)](o), Cs(+) caused a small inconsistent hyperpolarization and a net depolarization in quiescent fibers; and decreased MDP in driven fibers. In the presence of strophanthidin, Cs(+) hyperpolarized less. Increasing [Cs(+)](o) to 4, 8 and 16 mM gradually hyperpolarized less, depolarized more and abolished the undershoot. We conclude that in Purkinje fibers Cs(+) hyperpolarizes the membrane by stimulating the activity of the electrogenic Na(+)-K(+) pump (and not by suppressing I(f)), and blocks the pacemaker potential by blocking the undershoot, consistent with a Cs(+) block of a potassium pacemaker current. Copyright 1995 S. Karger AG, Basel
