Stimulation of the sodium pump by azide and high internal sodium: changes in the number of pumping sites and turnover rate.

Erlij, David; Grinstein, Sergio

doi:10.1113/jphysiol.1976.sp011453

Cited by 14 publications

(5 citation statements)

References 11 publications

(15 reference statements)

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“…This is surprising, in view of the fact that in muscles containing predominantly type II fibers, insulin stimulates active Na ϩ -K ϩ transport (122,302).…”

Section: Insulinmentioning

confidence: 94%

“…6) Depolarization of isolated muscles induced by high [K ϩ ] o , azide, or veratridine induces ouabain-suppressible stimulation of 22 Na efflux (122,127). The stimulating effect of high [K ϩ ] o was suppressed by TTX, indicating that depolarization stimulates the Na ϩ -K ϩ pump, but that the effect depends on the opening of Na ϩ channels.…”

Section: )mentioning

confidence: 95%

“…Stimulation of the Na ϩ -K ϩ pumps may also reflect an increase in the turnover number of the transport system. In skeletal muscle, this is likely to account for the acceleration induced by azide (122) or elevated temperature (79). Recent studies indicate that insulin increases the turnover number of the Na ϩ -K ϩ pumps in fibroblasts (279).…”

Section: E General Mechanisms For Acute Regulation Of the Na ؉ -K ؉ mentioning

confidence: 97%

“…In isolated frog sartorius muscle, insulin was reported to increase the binding of [ 3 H]ouabain, which was taken to indicate a mobilization of Na ϩ -K ϩ pumps to the membrane surface (122). However, the measurements of [ 3 H]ouabain binding were performed before it could be ascertained that all Na ϩ -K ϩ pumps were occupied.…”

Section: Insulinmentioning

confidence: 99%

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Na⁺-K⁺Pump Regulation and Skeletal Muscle Contractility

Clausen

2003

Physiological Reviews

514

673

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In skeletal muscle, excitation may cause loss of K+, increased extracellular K+ ([K+]o), intracellular Na+ ([Na+]i), and depolarization. Since these events interfere with excitability, the processes of excitation can be self-limiting. During work, therefore, the impending loss of excitability has to be counterbalanced by prompt restoration of Na+-K+ gradients. Since this is the major function of the Na+-K+ pumps, it is crucial that their activity and capacity are adequate. This is achieved in two ways: 1) by acute activation of the Na+-K+ pumps and 2) by long-term regulation of Na+-K+ pump content or capacity. 1) Depending on frequency of stimulation, excitation may activate up to all of the Na+-K+ pumps available within 10 s, causing up to 22-fold increase in Na+ efflux. Activation of the Na+-K+ pumps by hormones is slower and less pronounced. When muscles are inhibited by high [K+]o or low [Na+]o, acute hormone- or excitation-induced activation of the Na+-K+ pumps can restore excitability and contractile force in 10-20 min. Conversely, inhibition of the Na+-K+ pumps by ouabain leads to progressive loss of contractility and endurance. 2) Na+-K+ pump content is upregulated by training, thyroid hormones, insulin, glucocorticoids, and K+ overload. Downregulation is seen during immobilization, K+ deficiency, hypoxia, heart failure, hypothyroidism, starvation, diabetes, alcoholism, myotonic dystrophy, and McArdle disease. Reduced Na+-K+ pump content leads to loss of contractility and endurance, possibly contributing to the fatigue associated with several of these conditions. Increasing excitation-induced Na+ influx by augmenting the open-time or the content of Na+ channels reduces contractile endurance. Excitability and contractility depend on the ratio between passive Na+-K+ leaks and Na+-K+ pump activity, the passive leaks often playing a dominant role. The Na+-K+ pump is a central target for regulation of Na+-K+ distribution and excitability, essential for second-to-second ongoing maintenance of excitability during work.

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“…This is surprising, in view of the fact that in muscles containing predominantly type II fibers, insulin stimulates active Na ϩ -K ϩ transport (122,302).…”

Section: Insulinmentioning

confidence: 94%

Section: )mentioning

confidence: 95%

Section: E General Mechanisms For Acute Regulation Of the Na ؉ -K ؉ mentioning

confidence: 97%

Section: Insulinmentioning

confidence: 99%

See 2 more Smart Citations

Na⁺-K⁺Pump Regulation and Skeletal Muscle Contractility

Clausen

2003

Physiological Reviews

514

673

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“…Azide causes in creased intracellular sodium uptake by mus cle [7,10]. The effects on sodium efflux and intracellular sodium concentration ap pears to vary with the concentrations of azide used and the tissue.…”

Section: Discussionmentioning

confidence: 99%

Sodium-Dependent and Sodium-Independent Glutamine Transport in the Control of Ammoniagenesis in Rat Kidney

McFarlane‐Anderson¹,

Alleyne²

1978

Kidney Blood Press Res

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Our experiments show Na⁺-dependent and Na⁺-independent uptake of glutamine by renal cortical slices. In a Na⁺-containing buffer, sodium azide stimulates glutamine uptake and ammoniagenesis in slices from normal rats but has no effect on slices from acidotic rats. In Na⁺-free buffers azide does not alter ammoniagenesis or glutamine uptake by slices from normal rats but decrease both in slices from acidotic rats. Azide decreases ammoniagenesis in mitochondria from normal rats but increases it in mitochondria from acidotic rats. We conclude that azide stimulates Na⁺-dependent glutamine uptake and Na+-independent uptake may be stimulated by acidosis.

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