title: [Decrease in the electrogenic contribution of Na,K-ATPase and resting membrane potential as a possible mechanism of calcium ion accumulation in filaments of the rat musculus soleus subjected to the short-term gravity unloading].
abstract: After three days of hind limb unloading, the depolarization of muscle fibers from -71.0 +/- 0.5 mV to -66.8 +/- 0.7 mV as well as a decrease in muscle excitability and a trend to fatigue acceleration were observed. After hind limb unloading, the electrogenic contribution of the ouabain-sensitive alpha2 isoform of Na,K-ATPase, tested as depolarization due to the administration of 1 microM ouabain, decreased from 6.2 +/- 0.6 to 0.5 +/- 0.8 mV. The contribution of the ouabain-resistant alpha1 isoform, estimated as additional depolarization after the administration of 500 microM ouabain, decreased from 4.6 +/- 0.6 to 2.6 +/- 0.6 mV. After hind limb unloading, the fluorescence intensity of single muscle fibers loaded with Fluo-4-AM increased more than four times, indicating an increase in intracellular Ca2+ concentration. The effect was prevented by local delivery of nifedipine, which blocks L-type Ca2+ channels. These data suggest the existence of a selective mechanism of suppression of the alpha2-pump electrogenic contribution, which led to the depolarization of soleus muscle fibers after 3 days of hind limb unloading. The depolarization in turn may activate L-type Ca2+ channels, resulting in intracellular Ca2+ accumulation.
authors.forename: I I
authors.initials: II
authors.lastname: Krivoĭ
authors.forename: V V
authors.initials: VV
authors.lastname: Kravtsova
authors.forename: E G
authors.initials: EG
authors.lastname: Altaeva
authors.forename: I V
authors.initials: IV
authors.lastname: Kubasov
authors.forename: A V
authors.initials: AV
authors.lastname: Prokof'ev
authors.forename: T M
authors.initials: TM
authors.lastname: Drabkina
authors.forename: E E
authors.initials: EE
authors.lastname: Nikol'skiĭ
authors.forename: B S
authors.initials: BS
authors.lastname: Shenkman
mesh_terms: D000818:Animals; D002118:Calcium / Q000378:metabolism*; D002121:Calcium Channel Blockers / Q000494:pharmacology; D020746:Calcium Channels, L-Type / Q000502:physiology; D002413:Cations, Divalent; D066298:In Vitro Techniques; D007527:Isoenzymes / Q000502:physiology; D008297:Male; D008564:Membrane Potentials; D018485:Muscle Fibers, Skeletal / Q000378:metabolism; D018482:Muscle, Skeletal / Q000502:physiology*; D009543:Nifedipine / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D000254:Sodium-Potassium-Exchanging ATPase / Q000502:physiology*; D014893:Weightlessness
chemical_list: D002121:Calcium Channel Blockers; D020746:Calcium Channels, L-Type; D002413:Cations, Divalent; D007527:Isoenzymes; D000254:Sodium-Potassium-Exchanging ATPase; D009543:Nifedipine; D002118:Calcium