The Effect of Sodium Pump Blockade and Denervation on the Steady‐state Sodium Permeability of Mouse Skeletal Muscle Fibres

Seabrooke, S.R.; Ward, M. R.; White, Neal

doi:10.1113/expphysiol.1988.sp003176

Cited by 6 publications

(7 citation statements)

References 26 publications

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“…In the sartorius muscle of the frog and the diaphragm muscle of the rat, however, K+ can be reduced to at least 0.1 mm (Hodgkin & Horowicz, 1959) or even to ('nominally') potassium-free media (Hinke, 1987;Kuba & Nohmi, 1987) without depolarization. Other skeletal muscle cells do show the expected dichotomy in recorded Vm values when K+ is reduced (M0lgaard, Stiirup-Johansen & Flatman, 1980;Seabrooke, Ward & White, 1988;this paper). The present study shows that the dichotomy can be measured in a single cell.…”

Section: Introductionmentioning

confidence: 88%

Role of the anomalous rectifier in determining membrane potentials of mouse muscle fibres at low extracellular K+.

Heukelom

1991

The Journal of Physiology

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1. The membrane potential (Vm) of fibres of the extensor digitorum longus (EDL) of the mouse, measured at 35°C and with extracellular potassium concentration (K+) 57 mM, was Vm =-76 mV.2. Lowering K+ below 1 mm could lead to either a hyperpolarizing or a depolarizing response. When Vm was lower than -75-5 mV in the control medium, a reduction of K+ to 0-76 mm led to a hyperpolarization of Vm (-95 0 + 07 mV, n = 40); otherwise a depolarization occurred (Vm =-47-2+ 1'1 mV, n = 21).3. The difference in Vm responses did not correlate consistently with functional differences in cell types, as cells that originally hyperpolarized, could later depolarize.4. The observed phenomena could be explained if the properties of the anomalous rectifier, AR (or inward-going rectifier), are considered to be similar to those observed in cardiac cells.5. Apparently caesium acted as a competitive inhibitor; when the inhibition was strong enough the non-linear properties of the AR regeneratively amplified the depolarization to the full-blown depolarized state (Vm = -46'7 + 1-3 mV, n = 15). 6. Ouabain (10-4 M) reduced Vm (to -45+ 3 mV, n = 5) and reduced dramatically the selectivity of the cell membrane for potassium over sodium. These effects could be reversed readily by washing out the ouabain. 7. Adrenaline (2 /lM) added to the medium hyperpolarized Vm (AVm= -46 + 1-4 mV, n =9) and increased the changes induced by lowered K+ (from -14-3 + 05 mV, n = 5 to -180 + 08 mV, n = 9); the cells that originally depolarized when K+ was lowered could hyperpolarize after adrenaline addition.

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Section: Introductionmentioning

confidence: 88%

Role of the anomalous rectifier in determining membrane potentials of mouse muscle fibres at low extracellular K+.

Heukelom

1991

The Journal of Physiology

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“…Since barium blocks both Na + and K + channels, we perfused 8 hindlimbs with the voltage-sensitive Na + channel blocker TTX (Seabrooke et al 1988;Santana et al 1998) to discriminate between K + efflux through K + channels (most likely candidate) versus voltage-sensitive Na + channels. This was followed by 20 min of perfusion with TTX and 5 mM ouabain combined to determine if TTX-sensitive Na + chan-nels are involved in the ouabain-induced increase in unidirectional K + efflux.…”

Section: Tetrodotoxin and 5 MM Ouabain + Mm Tetrodotoxinmentioning

confidence: 99%

Section: Ouabain-induced K + Lossmentioning

confidence: 99%

“…In vitro, peak depolarizing effects (5-20 mV) have been observed with 1 mM ouabain (Clausen and Flatman 1977;Rogus et al 1977;Seabrooke et al 1988). Reductions in membrane potential may in turn affect voltage dependent ion channels (Seabrooke et al 1988) and other cellular proteins. The concept of altered ion selectivity of voltage-sensitive Na + channels has been introduced by Santana and colleagues (1998) who, using rat ventricular myocytes, demonstrated that cardiotonic steroids, including ouabain, were capable of increasing Ca 2+ flux through TTX-sensitive Na + channels.…”

Section: Ouabain-induced K + Lossmentioning

confidence: 99%

“…Although increased Na + channel conductance to K + in the presence of ouabain (or membrane depolarization) remains to be directly demonstrated, it is conceivable and supported by the present data. It has been demonstrated, too, that ouabain induces an increased membrane Na + permeability that is markedly prevented by treatment of muscles with TTX (Seabrooke et al 1988). …”

Section: Ouabain-induced K + Lossmentioning

confidence: 99%

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Ouabain stimulates unidirectional and net potassium efflux in resting mammalian skeletal muscle

Hawke

Lessard²,

Vickery³

et al. 2001

Can. J. Physiol. Pharmacol.

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The present study compared ouabain-sensitive unidirectional K+ flux into (JinK) and out of (JoutK) perfused rat hindlimb skeletal muscle in situ and mouse flexor digitorum brevis (FDB) in vitro. In situ, 5 mM ouabain inhibited 54 +/- 4% of the total JinK in 28 +/- 1 min, and increased the net and unidirectional efflux of K+ within 4 min. In contrast, 1.8 mM ouabain inhibited 40 +/- 8% of the total JinK in 38 +/- 2 min, but did not significantly affect JoutK. In vitro, 1.8 and 0.2 mM ouabain decreased JinK to a greater extent (83 +/- 5%) than in situ, but did not significantly affect 42K loss rate compared with controls. The increase in unidirectional K+ efflux (JoutK) with 5 mM ouabain in situ was attributed to increased K+ efflux through cation channels, since addition of barium (1 mM) to ouabain-perfused muscles returned JoutK to baseline values within 12 min. Perfusion with 5 mM ouabain plus 2 mM tetracaine for 30 min decreased JinK 46 +/- 9% (0.30 +/- 0.03 to 0.16 +/- 0.02 micromol x min(-1) x g(-1)), however tetracaine was unable to abolish the ouabain-induced increase in unidirectional K+ efflux. In both rat hindlimb and mouse FDB, tetracaine had no effect on JoutK. Perfusion of hindlimb muscle with 0.1 mM tetrodotoxin (TTX, a Na+ channel blocker) decreased JinK by 15 +/- 1%, but had no effect on JoutK; subsequent addition of ouabain (5 mM) decreased JinK a further 32 +/- 2%. The ouabain-induced increase in unidirectional K+ efflux did not occur when TTX was perfused prior to and during perfusion with 5 mM ouabain. We conclude that 5 mM ouabain increases the unidirectional efflux of K+ from skeletal muscle through a barium and TTX-sensitive pathway, suggestive of voltage sensitive Na+ channels, in addition to inhibiting Na+/K+-ATPase activity.

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Modelling action potentials and membrane currents of mammalian skeletal muscle fibres in coherence with potassium concentration changes in the T-tubular system

Wallinga

Meijer

Alberink

et al. 1999

European Biophysics Journal

114

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During prolonged activity the action potentials of skeletal muscle fibres change their shape. A model study was made as to whether potassium accumulation and removal in the tubular space is important with respect to those variations. Classical Hodgkin-Huxley type sodium and (potassium) delayed rectifier currents were used to determine the sarcolemmal and tubular action potentials. The resting membrane potential was described with a chloride conductance, a potassium conductance (inward rather than outward rectifier) and a sodium conductance (minor influence) in both sarcolemmal and tubular membranes. The two potassium conductances, the Na-K pump and the potassium diffusion between tubular compartments and to the external medium contributed to the settlement of the potassium concentration in the tubular space. This space was divided into 20 coupled concentric compartments. In the longitudinal direction the fibre was a cable series of 56 short segments. All the results are concerned with one of the middle segments. During action potentials, potassium accumulates in the tubular space by outward current through both the delayed and inward rectifier potassium conductances. In between the action potentials the potassium concentration decreases in all compartments owing to potassium removal processes. In the outer tubular compartment the diffusion-driven potassium export to the bathing solution is the main process. In the inner tubular compartment, potassium removal is mainly effected by re-uptake into the sarcoplasm by means of the inward rectifier and the Na-K pump. This inward transport of potassium strongly reduces the positive shift of the tubular resting membrane potential and the consequent decrease of the action potential amplitude caused by inactivation of the sodium channels. Therefore, both potassium removal processes maintain excitability of the tubular membrane in the centre of the fibre, promote excitation-contraction coupling and contribute to the prevention of fatigue.

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The Effect of Sodium Pump Blockade and Denervation on the Steady‐state Sodium Permeability of Mouse Skeletal Muscle Fibres

Cited by 6 publications

References 26 publications

Role of the anomalous rectifier in determining membrane potentials of mouse muscle fibres at low extracellular K+.

Role of the anomalous rectifier in determining membrane potentials of mouse muscle fibres at low extracellular K+.

Ouabain stimulates unidirectional and net potassium efflux in resting mammalian skeletal muscle

Modelling action potentials and membrane currents of mammalian skeletal muscle fibres in coherence with potassium concentration changes in the T-tubular system

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