title: Stretch-activated ion channels contribute to membrane depolarization after eccentric contractions.
abstract: We tested the hypothesis that eccentric contractions activate mechanosensitive or stretch-activated ion channels (SAC) in skeletal muscles, producing increased cation conductance. Resting membrane potentials and contractile function were measured in rat tibialis anterior muscles after single or multiple exposures to a series of eccentric contractions. Each exposure produced a significant and prolonged (>24 h) membrane depolarization in exercised muscle fibers. The magnitude and duration of the depolarization were related to the number of contractions. Membrane depolarization was due primarily to an increase in Na(+) influx, because the estimated Na(+)-to-K(+) permeability ratio was increased in exercised muscles and resting membrane potentials could be partially repolarized by substituting an impermeant cation for extracellular Na(+) concentration. Neither the Na(+)/H(+) antiport inhibitor amiloride nor the fast Na(+) channel blocker TTX had a significant effect on the depolarization. In contrast, addition of either of two nonselective SAC inhibitors, streptomycin or Gd(3+), produced significant membrane repolarization. The results suggest that muscle fibers experience prolonged depolarization after eccentric contractions due, principally, to the activation of Na(+)-selective SAC.
authors.affiliation: Department of Biology, California State University, Bakersfield 93311, USA.
authors.forename: T A
authors.initials: TA
authors.lastname: McBride
authors.forename: B W
authors.initials: BW
authors.lastname: Stockert
authors.forename: F A
authors.initials: FA
authors.lastname: Gorin
authors.forename: R C
authors.initials: RC
authors.lastname: Carlsen
mesh_terms: D000584:Amiloride / Q000494:pharmacology; D000818:Animals; D002412:Cations / Q000378:metabolism; D002463:Cell Membrane Permeability / Q000187:drug effects; D005260:Female; D005682:Gadolinium / Q000494:pharmacology; D007473:Ion Channels / Q000037:antagonists & inhibitors / Q000378:metabolism*; D008465:Mechanoreceptors / Q000378:metabolism*; D008536:Meglumine / Q000378:metabolism; D008564:Membrane Potentials / Q000187:drug effects; D009119:Muscle Contraction / Q000187:drug effects / Q000502:physiology*; D018485:Muscle Fibers, Skeletal / Q000187:drug effects / Q000502:physiology; D018482:Muscle, Skeletal / Q000166:cytology / Q000187:drug effects / Q000293:injuries / Q000502:physiology*; D010805:Physical Conditioning, Animal / Q000502:physiology*; D011188:Potassium / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D012964:Sodium / Q000378:metabolism; D026941:Sodium Channel Blockers; D015222:Sodium Channels / Q000378:metabolism; D017923:Sodium-Hydrogen Exchangers / Q000037:antagonists & inhibitors / Q000378:metabolism; D013307:Streptomycin / Q000494:pharmacology; D013779:Tetrodotoxin / Q000494:pharmacology
chemical_list: D002412:Cations; D007473:Ion Channels; D026941:Sodium Channel Blockers; D015222:Sodium Channels; D017923:Sodium-Hydrogen Exchangers; D013779:Tetrodotoxin; D008536:Meglumine; D000584:Amiloride; D012964:Sodium; D005682:Gadolinium; D011188:Potassium; D013307:Streptomycin