The Negative Inotropic Effect of Raised Extracellular Potassium and Caesium Ions on Isolated Frog Atrial Trabeculae

Abstract

SUMMARYThe exposure of frog atrial trabeculae to Ringer solution containing an elevated K+ concentration, produces a depolarization of the membrane and a reduction of both the duration of the action potential and the strength of the heart beat. In voltage-clamped preparations, the effect of perfusion with K+-rich Ringer solution is threefold. First, a sustained inward current develops at the holding potential (-80 mV). Secondly, the contractions evoked by depolarizing clamp pulses are reduced: this effect which is greater upon the tonic phase of the contraction than the early phasic tension, is also seen to follow the addition of Cs+ ions to the bathing fluid; at equal concentrations K+ ions are the more effective. Thirdly, when measured with an ionsensitive micro-electrode in ventricular trabeculae, the intracellular Na+ ion activity (aiN.) declines with a time course similar to the development of the negative inotropic effect. This suggests that the actions of raised [K+]. or [Cs+]o upon tension may be secondary to an effect on the movement of Na+ ions across the cell membrane, which by reducing aia may affect tension by way of the Na-Ca exchange.

Thermal sensitivity and phenotypic plasticity of cardiac mitochondrial metabolism in European perch, Perca fluviatilis

“…For example, while the decline of heart rate and cardiac contractility has previously been attributed to altered ionic trans-membrane ion conductance across the sarcolemma [owing to failing Na + channel function or a denaturation of Na + /K + -ATPase (Lennard and Huddart, 1991;Vornanen et al, 2014)], this may instead reflect an ATP limitation of Na + /K + -ATPase at high temperatures. Furthermore, impaired Na + /K + -ATPase activity may also lead to a reduced influx of K + , causing extracellular hyperkalemia, which further impairs myocardial conductivity, rhythmicity and contractility of hearts from fish and other ectotherms (Chapman and Rodrigo, 1987;Hove-Madsen and Gesser, 1989;Kalinin and Gesser, 2002;Nielsen and Gesser, 2001).…”

Effects of extracellular changes on spontaneous heart rate of normoxia-and anoxia-acclimated turtles (Trachemys scripta)

“…Indeed, in warmacclimated turtle hearts, extracellular acidosis decreases cardiac myocyte intracellular pH (Wasser et al, 1990a;Wasser et al, 1990b) and slows the maximum rate of force development during cardiac contraction Shi et al, 1999). Hyperkalemia reduces resting myocyte membrane potential (Nielsen and Gesser, 2001), which in mammals, negatively affects voltage-gated Ca 2+ channels and inactivates a proportion of the ventricular Na + channels, thereby slowing cardiac conduction (Chapman and Rodrigo, 1987;Bouchard et al, 2004). By contrast, hypercalcemia enhances the inward Ca 2+ gradient, and has been shown to alleviate the negative inotropic effects of hyperkalemia, acidosis or anoxia in warm-acclimated turtles (Yee and Jackson, 1984;Jackson, 1987;Nielsen and Gesser, 2001).…”

The role of adrenergic stimulation in maintaining maximum cardiac performance in rainbow trout (Oncorhynchus mykiss) during hypoxia,hyperkalemia and acidosis at 10°C

“…Hyperkalemia (10·mmol·l -1 and 12.5·mmol·l -1 K + ) reduces the contractive force of isolated heart strips bỹ 50% (Kalinin and Gesser, 2002) to ~100% (Nielsen and Gesser, 2001). Hyperkalemia reduces the resting membrane potential of myocardial cells (Chapman and Rodrigo, 1987;Hove-Madsen and Gesser, 1989), which in turn decreases the duration of the myocardial action potential, and thus the strength of myocardial contractions (Chapman and Rodrigo, 1987). Additionally, hyperkalemia in mammals (K + >5.5·mmol·l -1 ) has been shown to result in ventricular arrhythmia (Kes, 2001).…”