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    Por favor, use este identificador para citar o enlazar este ítem:http://uvadoc.uva.es/handle/10324/44482

    Título
    Differences in TRPC3 and TRPC6 channels assembly in mesenteric vascular smooth muscle cells in essential hypertension
    Autor
    Álvarez Miguel, InesAutoridad UVA Orcid
    Cidad Velasco, María Del PilarAutoridad UVA Orcid
    Pérez García, María TeresaAutoridad UVA Orcid
    López López, José RamónAutoridad UVA Orcid
    Año del Documento
    2016
    Editorial
    The Physiological Society
    Descripción
    Producción Científica
    Documento Fuente
    The Journal of Physiology, 2017, vol. 595, n. 5. p. 1497-1513
    Abstract
    Increased vascular tone in essential hypertension involves a sustained rise in total peripheral resistance. A model has been proposed in which the combination of membrane depolarization and higher L‐type Ca2+ channel activity generates augmented Ca2+ influx into vascular smooth muscle cells (VSMCs), contraction and vasoconstriction. The search for culprit ion channels responsible for membrane depolarization has provided several candidates, including members of the canonical transient receptor potential (TRPC) family. TRPC3 and TRPC6 are diacylglycerol‐activated, non‐selective cationic channels contributing to stretch‐ or agonist‐induced depolarization. Conflicting information exists regarding changes in TRPC3/TRPC6 functional expression in hypertension. However, although TRPC3‐TRPC6 channels can heteromultimerize, the possibility that differences in their association pattern may change their functional contribution to vascular tone is largely unexplored. We probe this hypothesis using a model of essential hypertension (BPH mice; blood pressure high) and its normotensive control (BPN mice; blood pressure normal). First, non‐selective cationic currents through homo‐ and heterotetramers recorded from transfected Chinese hamster ovary cells indicated that TRPC currents were sensitive to the selective antagonist Pyr10 only when TRPC6 was present, whereas intracellular anti‐TRPC3 antibody selectively blocked TRPC3‐mediated currents. In mesenteric VSMCs, basal and agonist‐induced currents were more sensitive to Pyr3 and Pyr10 in BPN cells. Consistently, myography studies showed a larger Pyr3/10‐induced vasodilatation in BPN mesenteric arteries. mRNA and protein expression data supported changes in TRPC3 and TRPC6 proportions and assembly, with a higher TRPC3 channel contribution in BPH VSMCs that could favour cell depolarization. These differences in functional and pharmacological properties of TRPC3 and TRPC6 channels, depending on their assembly, could represent novel therapeutical opportunities.
    Palabras Clave
    Arterial smooth muscle
    Músculo liso vascular
    Hypertension
    Hipertensión
    ISSN
    1469-7793
    Revisión por pares
    SI
    DOI
    10.1113/JP273327
    Patrocinador
    Instituto de Salud Carlos III (project RD12/0042/0006)
    Programa Estatal de Investigación (project BFU2013-45867-R )
    Version del Editor
    https://physoc.onlinelibrary.wiley.com/doi/abs/10.1113/JP273327
    Propietario de los Derechos
    © 2016 The Physiological Society
    Idioma
    eng
    URI
    http://uvadoc.uva.es/handle/10324/44482
    Tipo de versión
    info:eu-repo/semantics/publishedVersion
    Derechos
    openAccess
    Collections
    • DEP06 - Artículos de revista [352]
    • IBGM - Artículos de revista [78]
    • VASCUMIT - Artículos de revista [47]
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    Attribution-NonCommercial-NoDerivatives 4.0 InternacionalExcept where otherwise noted, this item's license is described as Attribution-NonCommercial-NoDerivatives 4.0 Internacional

    Universidad de Valladolid

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