Excitation- and beta(2)-agonist-induced activation of the Na(+)-K(+) pump in rat soleus muscle.
In rat skeletal muscle, Na(+)-K(+) pump activity increases dramatically in response to excitation (up to 20-fold) or beta(2)-agonists (2-fold), leading to a reduction in intracellular Na(+). This study examines the time course of these effects and whether they are due to an increased affinity of the Na(+)-K(+) pump for intracellular Na(+). Isolated rat soleus muscles were incubated at 30 (o)C in Krebs-Ringer bicarbonate buffer. The effects of direct electrical stimulation on (86)Rb(+) uptake rate and intracellular Na(+) concentration ([Na(+)](i)) were characterized in the subsequent recovery phase. [Na(+)](i) was varied using monensin or buffers with low Na(+). In the [Na(+)](i) range 21-69 mM, both the beta(2)-agonist salbutamol and electrical stimulation produced a left shift of the curves relating (86)Rb(+) uptake rate to [Na(+)](i). In the first 10 s after 1 or 10 s pulse trains of 60 Hz, [Na(+)](i) showed no increase, but (86)Rb(+) uptake rate increased by 22 and 86 %, respectively. Muscles excited in Na(+)-free Li(+)-substituted buffer and subsequently allowed to rest in standard buffer also showed a significant increase in (86)Rb(+) uptake rate and decrease in [Na(+)](i). Na(+) loading induced by monensin or electroporation also stimulated (86)Rb(+) uptake rate but, contrary to excitation, increased [Na(+)](i). The increase in the rate of (86)Rb(+) uptake elicited by electrical stimulation was abolished by ouabain, but not by bumetanide. The results indicate that excitation (like salbutamol) induces a rapid increase in the affinity of the Na(+)-K(+) pump for intracellular Na(+). This leads to a Na(+)-K(+) pump activation that does not require Na(+) influx, but possibly the generation of action potentials. This improves restoration of the Na(+)-K(+) homeostasis during work and optimizes excitability and contractile performance of the working muscle.
Buchanan
Rasmus
R
Department of Physiology, University of Aarhus, DK-8000 Aarhus C, Denmark.
Nielsen
Ole Baekgaard
OB
Clausen
Torben
T
D000318:Adrenergic beta-Agonists / Q000494:pharmacology*; D000420:Albuterol / Q000494:pharmacology*; D000818:Animals; D004558:Electric Stimulation; D018274:Electroporation; D005260:Female; D066298:In Vitro Techniques; D007425:Intracellular Membranes / Q000378:metabolism; D008297:Male; D018482:Muscle, Skeletal / Q000187:drug effects* / Q000502:physiology*; D009994:Osmolar Concentration; D051381:Rats; D017208:Rats, Wistar; D012413:Rubidium / Q000493:pharmacokinetics; D012964:Sodium / Q000378:metabolism; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism*
D000318:Adrenergic beta-Agonists; D012964:Sodium; D000254:Sodium-Potassium-Exchanging ATPase; D012413:Rubidium; D000420:Albuterol