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Excitation- and ₂-agonist-induced activation of the Na⁺-K⁺ pump in rat soleus muscle

Rasmus Buchanan, Ole Bækgaard Nielsen and Torben Clausen

In rat skeletal muscle, Na⁺-K⁺ pump activity increases dramatically in response to excitation (up to 20-fold) or 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 ^oC in Krebs-Ringer bicarbonate buffer. The effects of direct electrical stimulation on ⁸⁶Rb⁺ 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 ₂-agonist salbutamol and electrical stimulation produced a left shift of the curves relating ⁸⁶Rb⁺ 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 ⁸⁶Rb⁺ 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 ⁸⁶Rb⁺ uptake rate and decrease in [Na⁺]_i. Na⁺ loading induced by monensin or electroporation also stimulated ⁸⁶Rb⁺ uptake rate but, contrary to excitation, increased [Na⁺]_i. The increase in the rate of ⁸⁶Rb⁺ 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.

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