Changes in extracellular K⁺ concentration modulate contractility of rat and rabbit cardiac myocytes via the inward rectifier K⁺ current I_K1

Abstract

The mechanisms underlying the inotropic effect of reductions in [K

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).…”

Modulation of membrane potential by an acetylcholine-activated potassium current in trout atrial myocytes

“…It also favors calcium removal from the cytosol by forward mode electrogenic Na ϩ /Ca 2ϩ exchange and, thus, relaxation of contraction. The role of specific potassium channels in the repolarization and maintenance of the resting membrane potential has been extensively studied in mammalian cardiac myocytes (3,5,8,18,24). However, the mechanisms regulating repolarization and the maintenance of the resting membrane potential in the fish heart needs clarification.…”

“…In the mammalian heart, the resting potential is primarily determined by the inwardly rectifying potassium current (I K1 ), and this current has also been proposed to set the resting potential in teleost myocytes (3,31). Several other currents have been shown to modulate the resting potential in mammalian cardiac myocytes (3,8,19,22,25). The ACh-activated I K (I K,ACh ) has been shown to modulate the membrane potential in mammalian atrial and, to a lesser extent, ventricular cells (19).…”

Experimental study on inhibition of rat ventricular Ik1 by RNA interference targeting the KCNJ2 gene

“…When the membrane potential is lower than the potential for K + equilibrium, an inward current is generated. This plays a leading role in maintaining the resting potential and in the potassium sensitivity of cells (17). At the end of complex polarization, most channels are inactivated and I K1 is activated, facilitating rapid complex polarization and inhibiting early after-depolarization (18).…”