Modulation of the isoprenaline‐induced membrane hyperpolarization of mouse skeletal muscle cells

Abstract

1 The hyperpolarization of the resting membrane potential, V., induced by isoprenaline in the lumbrical muscle fibres of the mouse, was investigated by use of intracellular microelectrodes.2 In normal Krebs-Henseleit solution (potassium concentration: K+= 5.7 mM, 'control'), V. was -74.0±0.2 mV; lowering K+ to 0.76 mM ('low K'7) resulted in either a hyperpolarization (VM -95.7± 2.9 mV), or a depolarization (Vm= -52.0± 0.3 mV). When Vm hyperpolarized after switching to low K', the addition of isoprenaline resulted in increased hyperpolarization Vm: AVm=-16.3 + 3.2 mV to a final Vm=-110.1I±3.4 mV. Adding iso-prenaline when Vm depolarized in low K+, leads to a hyperpolarization of either by -11.6 ± 0.5 mV to -63.6+0.8 mV or by -51.7+2.7 mV to -106.9±3.9 mV. 5 Ouabain (0.1 to 1 mM) did not suppress the hyperpolarization by isoprenaline in 5.7 mM K + (AVm=-6.7±0.4 mV) or the hyperpolarization of the depolarized cells in low K + (AVm= 9.7 ±1.5 mV). 6The hyperpolarization is a logarithmically decreasing function of K + in the range between 2 and 20 mM (12 mV/decade). 7 IBMX and 8Br-cyclic AMP mimicked the response to isoprenaline whereas forskolin (FSK) induced in low K + a hyperpolarization of -7.0±0.7 mV that could be augmented by addition of isoprenaline (AVm -8.2± 1.8 mV). 8In control and low K+, Ba2`(0.6 mM) inhibited the hyperpolarization induced by isoprenaline, IBMX or 8Br-cyclic AMP. Other blockers of the potassium conductance such as TEA (5 mM) and apamin (0.4 riM) had no effect. 9 We conclude that in the lumbrical muscle of the mouse the isoprenaline-induced hyperpolarization is primarily due to an increase in potassium permeability.

Effects of chloride transport on bistable behaviour of the membrane potential in mouse skeletal muscle

“…The reduced potassium permeability mentioned by Gallant (1983) can be interpreted as the closure of the K IR . Along with our earlier observations (Siegenbeek van Heukelom, 1991, 1994; Van Mil et al 1995), we conclude that our present observations might provide additional insight into hypokalaemic periodic paralysis (Barchi, 1994). At lower temperatures, as is the case in the body extremities, the closure of K IR will be most marked.…”

Lower Ca2+ enhances the K+-induced force depression in normal and HyperKPP mouse muscles

“…The hyperpolarization was associated with small increases in membrane excitability and action potential amplitude that are too small to explain the large force recovery. Activation of β2-adrenergic receptors also leads to Ca V 1.1 channel and ryanodine receptor phosphorylation (Curtis and Catterall, 1985;Suko et al, 1993;Cairns and Borrani, 2015), resulting in greater Ca 2+ release (Cairns et al, 1993;Bruton et al, 1996;Liu et al, 1997;Rudolf et al, 2006;Cairns and Borrani, 2015). It is therefore most likely that most of the force recovery at high K + in the presence of salbutamol is due to greater Ca 2+ release and to a lesser extent to a hyperpolarization (at 0.3 mM Ca 2+ ).…”

The role of K+ channels in the force recovery elicited by Na+‐K+ pump stimulation in Ba2+‐paralysed rat skeletal muscle

“…It is well‐documented that catecholamines, β 2 ‐adrenoceptor agonists and/or CGRP induce hyperpolarization in skeletal muscle (Tashiro, 1973; Clausen & Flatman, 1977; Andersen & Clausen, 1993; van Mil et al 1995), cardiac myocytes (Gadsby, 1983; Glitsch et al 1989) and vascular smooth muscle cells (for review, see Standen & Quayle, 1998). In skeletal muscle, this effect has often been attributed to cAMP‐mediated stimulation of the electrogenic Na + ‐K + pump (Clausen & Flatman, 1977; Andersen & Clausen, 1993; Li & Sperelakis, 1993).…”

“…In heart and smooth muscle, however, the hyperpolarization induced by catecholamines and CGRP is thought to reflect the opening of K + channels, mediated by cyclic AMP (Glitsch et al 1989; Standen & Quayle, 1998). It has been proposed that this is also the mechanism in skeletal muscle (van Mil et al 1995).…”