1995Journal of Biomedical ScienceRequires access

Cesium, Na^+-K^+ Pump and Pacemaker Potential in Cardiac Purkinje Fibers

Jeffrey P. Sternlicht, Mario Vasalle

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Abstract

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 If), 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 elec- trogenic 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.

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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 If), 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 elec- trogenic 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.

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Available abstract

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 If), 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 elec- trogenic 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.

Key concepts: Diastolic depolarization, Hyperpolarization (physics), Depolarization, Purkinje fibers, Pacemaker potential, Membrane potential, Chemistry, Biophysics

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