title: Regulation of Na(+)-K+ pump activity in contracting rat muscle.
abstract: 1. In rat soleus muscle, high frequency electrical stimulation produced a rapid increase in intracellular Na+ (Na+i) content. This was considerably larger in muscles contracting without developing tension than in muscles contracting isometrically. During subsequent rest a net extrusion of Na+ took place at rates which, depending on the frequency and duration of stimulation, approached the maximum transport capacity of the Na(+)-K+ pumps present in the muscle. 2. In isometrically contracting muscles, the net extrusion of Na+ continued for up to 10 min after stimulation, reducing Na+i to values 30% below the resting level (P < 0.001). This undershoot in Na+i, seen in both soleus and extensor digitorum longus muscles, could be maintained for up to 30 min and was blocked by ouabain or cooling to 0 degree C. 3. The undershoot in Na+i could be elicited by direct stimulation as well as by tubocurarine-suppressible stimulation via the motor endplate. It could not be attributed to a decrease in Na+ influx, to effects of noradrenaline or calcitonin gene-related peptide released from nerve endings, to an increase in extracellular K+ or the formation of nitric oxide. 4. The results indicate that excitation rapidly activates the Na(+)-K+ pump, partly via a change in its transport characteristics and partly via an increase in intracellular Na+ concentration. This activation allows an approximately 20-fold increase in the rate of Na+ efflux to take place within 10 s. 5. The excitation-induced activation of the Na(+)-K+ pump may represent a feed-forward mechanism that protects the Na(+)-K+ gradients and the membrane potential in working muscle. Contrary to previous assumptions, the Na(+)-K+ pump seems to play a dynamic role in maintenance of excitability during contractile activity.
authors.affiliation: Department of Physiology, University of Aarhus, Denmark. obn@fi.aau.dk
authors.forename: O B
authors.initials: OB
authors.lastname: Nielsen
authors.forename: T
authors.initials: T
authors.lastname: Clausen
mesh_terms: D000420:Albuterol / Q000494:pharmacology; D000818:Animals; D015740:Calcitonin Gene-Related Peptide / Q000494:pharmacology; D003080:Cold Temperature; D003620:Dantrolene / Q000494:pharmacology; D004558:Electric Stimulation; D004791:Enzyme Inhibitors / Q000494:pharmacology; D007537:Isometric Contraction / Q000187:drug effects / Q000502:physiology*; D008297:Male; D018485:Muscle Fibers, Skeletal / Q000737:chemistry / Q000187:drug effects / Q000201:enzymology; D009125:Muscle Relaxants, Central / Q000494:pharmacology; D018482:Muscle, Skeletal / Q000166:cytology / Q000502:physiology*; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D018733:Nicotinic Antagonists / Q000494:pharmacology; D011433:Propranolol / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D012530:Saxitoxin / Q000494:pharmacology; D012964:Sodium / Q000378:metabolism; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism*; D013565:Sympatholytics / Q000494:pharmacology; D013566:Sympathomimetics / Q000494:pharmacology; D014403:Tubocurarine / Q000494:pharmacology
chemical_list: D004791:Enzyme Inhibitors; D009125:Muscle Relaxants, Central; D018733:Nicotinic Antagonists; D013565:Sympatholytics; D013566:Sympathomimetics; D012530:Saxitoxin; D012964:Sodium; D011433:Propranolol; D000254:Sodium-Potassium-Exchanging ATPase; D003620:Dantrolene; D015740:Calcitonin Gene-Related Peptide; D000420:Albuterol; D019331:NG-Nitroarginine Methyl Ester; D014403:Tubocurarine