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Cellular Na+ handling mechanisms involved in airway smooth muscle contraction (Review)

  • Authors:
    • Bettina Sommer
    • Edgar Flores-Soto
    • Georgina Gonzalez-Avila
  • View Affiliations / Copyright

    Affiliations: Department of Bronchial Hyperreactivity, National Institute of Respiratory Diseases ‘Ismael Cosio Villegas’, CP 14080 Mexico City, Mexico, Department of Pharmacology, Faculty of Medicine, National Autonomous University of Mexico, CP 04510 Mexico City, Mexico, Biomedical Oncology Laboratory, Department of Chronic‑Degenerative Diseases, National Institute of Respiratory Diseases ‘Ismael Cosio Villegas’, CP 14080 Mexico City, Mexico
    Copyright: © Sommer et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 3-9
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    Published online on: May 17, 2017
       https://doi.org/10.3892/ijmm.2017.2993
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Abstract

A decrease in bronchial diameter is designated as bronchoconstriction (BC) and impedes the flow of air through the airway. Asthma is characterized by inflammation of the airways, reversible BC and nonspecific hyperreactivity. These last two symptoms are dependent on airway smooth muscle. Stimuli that trigger contraction can be characterized as chemical (neurotransmitters, cytokines and terpenoids) and physical (volume inspired, air pressure). Both stimuli activate signaling pathways by acting on membrane proteins and facilitating the passage of ions through the membrane, generating a voltage change and a subsequent depolarization. Na+ plays an important role in preserving the resting membrane potential; this ion is extracted from the cells by the Na+/K+ ATPase (NKA) or introduced into the cytoplasm by the Na+/Ca2+ exchanger (NCX). During depolarization, Na+ appears to accumulate in specific regions beneath the plasma membrane, generating local concentration gradients which determine the handling of Ca2+. At rest, the smooth muscle has a basal tone that is preserved by the continuous adjustment of intracytoplasmic concentrations of Ca2+ and Na+. At homeostasis, the Na+ concentration is primarily dependent on three structures: the NKA, the NCX and non-specific cation channels (NSCC). These three structures, their functions and the available evidence of the probable role of Na+ in asthma are described in the present review.
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Copy and paste a formatted citation
Spandidos Publications style
Sommer B, Flores-Soto E and Gonzalez-Avila G: Cellular Na+ handling mechanisms involved in airway smooth muscle contraction (Review). Int J Mol Med 40: 3-9, 2017.
APA
Sommer, B., Flores-Soto, E., & Gonzalez-Avila, G. (2017). Cellular Na+ handling mechanisms involved in airway smooth muscle contraction (Review). International Journal of Molecular Medicine, 40, 3-9. https://doi.org/10.3892/ijmm.2017.2993
MLA
Sommer, B., Flores-Soto, E., Gonzalez-Avila, G."Cellular Na+ handling mechanisms involved in airway smooth muscle contraction (Review)". International Journal of Molecular Medicine 40.1 (2017): 3-9.
Chicago
Sommer, B., Flores-Soto, E., Gonzalez-Avila, G."Cellular Na+ handling mechanisms involved in airway smooth muscle contraction (Review)". International Journal of Molecular Medicine 40, no. 1 (2017): 3-9. https://doi.org/10.3892/ijmm.2017.2993
Copy and paste a formatted citation
x
Spandidos Publications style
Sommer B, Flores-Soto E and Gonzalez-Avila G: Cellular Na+ handling mechanisms involved in airway smooth muscle contraction (Review). Int J Mol Med 40: 3-9, 2017.
APA
Sommer, B., Flores-Soto, E., & Gonzalez-Avila, G. (2017). Cellular Na+ handling mechanisms involved in airway smooth muscle contraction (Review). International Journal of Molecular Medicine, 40, 3-9. https://doi.org/10.3892/ijmm.2017.2993
MLA
Sommer, B., Flores-Soto, E., Gonzalez-Avila, G."Cellular Na+ handling mechanisms involved in airway smooth muscle contraction (Review)". International Journal of Molecular Medicine 40.1 (2017): 3-9.
Chicago
Sommer, B., Flores-Soto, E., Gonzalez-Avila, G."Cellular Na+ handling mechanisms involved in airway smooth muscle contraction (Review)". International Journal of Molecular Medicine 40, no. 1 (2017): 3-9. https://doi.org/10.3892/ijmm.2017.2993
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