Na(+) permeates through L-type Ca(2+) channel in bovine airway smooth muscle

Membrane depolarization of airway smooth muscle (ASM) opens L-type voltage dependent Ca(2+) channels (L-VDCC) allowing Ca(2+) entrance to produce contraction. In Ca(2+) free conditions Na(+) permeates through L-VDCC in excitable and non-excitable cells and this phenomenon is annulled at µM Ca(2+) co...

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Bibliographic Details
Published in:European journal of pharmacology 2016-07, Vol.782, p.77-88
Main Authors: Sommer, Bettina, Flores-Soto, Edgar, Reyes-García, Jorge, Díaz-Hernández, Verónica, Carbajal, Verónica, Montaño, Luis M
Format: Article
Language:English
Subjects:
Animals
Calcium Channels, L-Type - genetics
Calcium Channels, L-Type - metabolism
Cattle
Cell Membrane - metabolism
Gene Expression Regulation
Muscle, Smooth - cytology
Muscle, Smooth - metabolism
Permeability
Sarcoplasmic Reticulum - metabolism
Sodium - metabolism
Trachea - metabolism
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Summary:Membrane depolarization of airway smooth muscle (ASM) opens L-type voltage dependent Ca(2+) channels (L-VDCC) allowing Ca(2+) entrance to produce contraction. In Ca(2+) free conditions Na(+) permeates through L-VDCC in excitable and non-excitable cells and this phenomenon is annulled at µM Ca(2+) concentrations. Membrane depolarization also induces activation of Gq proteins and sarcoplasmic reticulum Ca(2+) release. In bovine ASM, KCl induced a transient contraction sensitive to nifedipine in Ca(2+)free medium, indicating an additional mechanism to the SR-Ca(2+) release. It is possible that Na(+) could permeate through L-VDCC in bovine ASM. KCl induced a transient contraction in Ca(2+) free medium with a fast intracellular Ca(2+) increment, reduced by TMB-8. This contraction was abolished by caffeine and CPA, diminished with nifedipine and augmented by Bay K8644. Increasing extracellular Na(+) concentration in tracheal myocytes, proportionally augmented the SBFI fluorescence ratio, suggesting an increment in the intracellular Na(+) concentration ([Na(+)]i). 50mM Na(+) with and without Ca(2+) induced a [Na(+)]i increment, enhanced by Bay K8644 and inhibited with D-600. In Ca(2+) free medium, KCl increased [Na(+)]i. Ba(2+) currents corresponding to L-VDCC were observed in myocytes and Na(+) permeated in the presence and absence of Ca(2+). SBFI-loaded myocytes in Na(+) and Ca(2+) containing Krebs stimulated with carbachol showed a Na(+) increment with a plateau. D-600 and 2-APB almost abolished the carbachol-induced Na(+) increment. RT-PCR demonstrated that CaV1.2 is the only L-VDCC subunit present in ASM. under physiological conditions, Na(+) permeates through L-VDCC in bovine ASM, probably contributing to sustain membrane depolarization during agonist stimulation.
ISSN:1879-0712
DOI:10.1016/j.ejphar.2016.04.040