Stretch-activated ion channels contribute to membrane depolarization after eccentric contractions.
J Appl Physiol (1985)
; 88(1): 91-101, 2000 Jan.
Article
en En
| MEDLINE
| ID: mdl-10642367
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.
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Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Condicionamiento Físico Animal
/
Músculo Esquelético
/
Canales Iónicos
/
Mecanorreceptores
/
Contracción Muscular
Límite:
Animals
Idioma:
En
Revista:
J Appl Physiol (1985)
Asunto de la revista:
FISIOLOGIA
Año:
2000
Tipo del documento:
Article
País de afiliación:
Estados Unidos