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    Vascular control of the CO2/H+ dependent drive to breathe

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    Author
    Cleary, Colin M.
    Moreira, Thiago S.
    Takakura, Ana C.
    Nelson, Mark T.
    Longden, Thomas A.
    Mulkey, Daniel K.
    Date
    2020-09-14
    Journal
    eLife
    Publisher
    eLife Sciences Publications
    Type
    Article
    
    Metadata
    Show full item record
    See at
    https://doi.org/10.7554/ELIFE.59499
    Abstract
    Respiratory chemoreceptors regulate breathing in response to changes in tissue CO2/ H+. Blood flow is a fundamental determinant of tissue CO2/H+, yet little is known regarding how regulation of vascular tone in chemoreceptor regions contributes to respiratory behavior. Previously, we showed in rat that CO2/H+-vasoconstriction in the retrotrapezoid nucleus (RTN) supports chemoreception by a purinergic-dependent mechanism (Hawkins et al., 2017). Here, we show in mice that CO2/H+ dilates arterioles in other chemoreceptor regions, thus demonstrating CO2/H+ vascular reactivity in the RTN is unique. We also identify P2Y2 receptors in RTN smooth muscle cells as the substrate responsible for this response. Specifically, pharmacological blockade or genetic deletion of P2Y2 from smooth muscle cells blunted the ventilatory response to CO2, and re-expression of P2Y2 receptors only in RTN smooth muscle cells fully rescued the CO2/H+ chemoreflex. These results identify P2Y2 receptors in RTN smooth muscle cells as requisite determinants of respiratory chemoreception.
    Sponsors
    American Heart Association
    Keyword
    astrocyte
    chemoreception
    functional vascular heterogeneity
    mouse
    neuroscience
    neurovascular unit
    retrotrapezoid nucleus
    Identifier to cite or link to this item
    http://hdl.handle.net/10713/13884
    ae974a485f413a2113503eed53cd6c53
    10.7554/eLife.59499
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