Interrelation of hypokalaemia and potassium depletion and its implications: a re-evaluation based on studies of the skeletal muscle sodium, potassium-pump

1991 ◽  
Vol 81 (s25) ◽  
pp. 449-455 ◽  
Author(s):  
Aage Nørgaard ◽  
Keld Kjeldsen
Keyword(s):  
Skeletal Muscle ◽  
Potassium Depletion ◽  
Sodium Potassium ◽  
Sodium Potassium Pump

The dual nature of the membrane potential increase associated with the activity of the sodium/potassium exchange pump in skeletal muscle fibres

1977 ◽  
Vol 198 (1133) ◽  
pp. 463-472 ◽  
Keyword(s):  
Skeletal Muscle ◽  
Membrane Potential ◽  
Muscle Fibres ◽  
Potassium Depletion ◽  
Sodium Potassium ◽  
Dual Nature ◽  
Tubular System ◽  
Pump Activity ◽  
Skeletal Muscle Fibres ◽  
Potassium Exchange

Results are presented which suggest that the contribution to the membrane potential in frog skeletal muscle evoked by ionic pump activity is made up of two components. One of these is directly related to the ‘electrogenic’ mode of pump action; the other, of similar magnitude, is an indirect effect due to potassium depletion in the lumen of the T -tubular system. The extent of this depletion has been estimated.

Hypothalamic regulation of sodium-potassium pump activity in skeletal muscle

1986 ◽  
Vol 384 (1) ◽  
pp. 17-22 ◽  
Author(s):  
Hironobu Yoshimatsu ◽  
Yutaka Oomura ◽  
Toshihiko Katafuchi ◽  
Norio Akaike
Keyword(s):  
Skeletal Muscle ◽  
Sodium Potassium ◽  
Pump Activity ◽  
Hypothalamic Regulation ◽  
Sodium Potassium Pump

Effect of palytoxin on the sodium–potassium pump: model and simulation

2008 ◽  
Vol 5 (3) ◽  
pp. 036005 ◽  
Author(s):  
Antônio M Rodrigues ◽  
Antônio-Carlos G Almeida ◽  
Antonio F C Infantosi
Keyword(s):  
Sodium Potassium ◽  
Model And Simulation ◽  
Sodium Potassium Pump

An integrative, in situ approach to examining K+ flux in resting skeletal muscle

2001 ◽  
Vol 79 (12) ◽  
pp. 996-1006 ◽  
Author(s):  
Michael I Lindinger ◽  
Thomas J Hawke ◽  
Lisa Vickery ◽  
Laurie Bradford ◽  
Shonda L Lipskie
Keyword(s):  
Skeletal Muscle ◽  
Drug Effects ◽  
Potassium Transport ◽  
Mammalian Skeletal Muscle ◽  
Minimal Effect ◽  
Bovine Erythrocyte ◽  
Perfusion Medium ◽  
Sodium Potassium ◽  
Unidirectional Flux

The contributions of Na+/K+-ATPase, K+ channels, and the NaK2Cl cotransporter (NKCC) to total and unidirectional K+ flux were determined in mammalian skeletal muscle at rest. Rat hindlimbs were perfused in situ via the femoral artery with a bovine erythrocyte perfusion medium that contained either 86Rb or 42K, or both simultaneously, to determine differences in ability to trace unidirectional K+ flux in the absence and presence of K+-flux inhibitors. In most experiments, the unidirectional flux of K+ into skeletal muscle (JinK) measured using 86Rb was 8–10% lower than JinK measured using 42K. Ouabain (5 mM) was used to inhibit Na+/K+-ATPase activity, 0.06 mM bumetanide to inhibit NKCC activity, 1 mM tetracaine or 0.5 mM barium to block K+ channels, and 0.05 mM glybenclamide (GLY) to block ATP-sensitive K+ (KATP) channels. In controls, JinK remained unchanged at 0.31 ± 0.03 µmol·g–1·min–1 during 55 min of perfusion. The ouabain-sensitive Na+/K+-ATPase contributed to 50 ± 2% of basal JinK, K+ channels to 47 ± 2%, and the NKCC to 12 ± 1%. GLY had minimal effect on JinK, and both GLY and barium inhibited unidirectional efflux of K+ (JoutK) from the cell through K+ channels. Combined ouabain and tetracaine reduced JinK by 55 ± 2%, while the combination of ouabain, tetracaine, and bumetanide reduced JinK by 67 ± 2%, suggesting that other K+-flux pathways may be recruited because the combined drug effects on inhibiting JinK were not additive. The main conclusions are that the NKCC accounted for about 12% of JinK, and that KATP channels accounted for nearly all of the JoutK, in resting skeletal muscle in situ.Key words: sodium potassium chloride cotransporter, NKCC, Na+/K+-ATPase, potassium channels, potassium transport, in situ rat hindlimb.

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