Cesium (5-25 mM) depolarized the resting potential, reduced delayed outward current, and produced a dose-dependent slowing of repetitive firing in mammalian ventricular myocardium.
Cesium blockade of outward pacemaker currents slows pacemaker activity in mammalian ventricular myocardium.
The effects of Cs+, 5-25 mM, were studied in cat and guinea pig papillary muscles using voltage clamp and current clamp techniques. In solutions containing normal K+, the major effects of Cs+ were depolarization of the resting potential and reduction of the delayed outward current (ixl) between -80 and -20 mV. Both inward and outward portions of the isochronal current voltage relation (l-s clamps) were reduced by extracellular Cs+. This resulted in a substantial reduction of inward rectification and, by subtraction from the normal I-V relationship, the definition of a Cs+-sensitive component of current. Under current clamp conditions, 5-10 mM Cs+ produced a dose-dependent slowing of repetitive firing induced by depolarization. At higher concentrations (25 mM) the resting potential was depolarized and repetitive activity could not be induced by further depolarization. However, release of hyperpolarizing pulses was followed by prolonged bursts of repetitive action potentials, suggesting partial reversal of blockade or participation of another pacemaker process. The experimental results and a numerical simulation show that under readily attainable conditions, reduction in an outward pacemaker current may slow pacemaker activity.
Meier et al. (Fri,) reported a other. Cesium (Cs+) vs. Normal K+ solutions was evaluated on Electrophysiological effects (depolarization of resting potential, reduction of delayed outward current, slowing of repetitive firing). Cesium (5-25 mM) depolarized the resting potential, reduced delayed outward current, and produced a dose-dependent slowing of repetitive firing in mammalian ventricular myocardium.