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Hypoxic regulation of Ca2+ signalling in astrocytes and endothelial cells

Peers, Chris, Aley, Parvinder, K., Boyle, John P., Porter, Karen E., Pearson, Hugh A., Smith, Ian F. and Kemp, Paul J. 2006. Hypoxic regulation of Ca2+ signalling in astrocytes and endothelial cells. In: Hayashida, Yoshiaki, Gonzalez, Constancio and Konda, Hisataki eds. The Arterial Chemoreceptors, Vol. 580. Advances in Experimental Medicine and Biology, Kluwer, pp. 185-190. (10.1007/0-387-31311-7_28)

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Hypoxic modulation of K+ channels is now firmly established in a variety of tissue types (Lopez-Barneo et al., 1988; Weir and Archer, 1998; Franco- Obregon et al., 1995; Youngson et al., 1993; Hool, 2001; Jiang and Haddad, 1994; Rychkov et al., 1998), and hypoxic modulation of specific channel types can also be reproduced in recombinant expression systems (Fearon et al., 2000; Lewis et al., 2001; Lewis et al., 2002; Williams et al., 2004), providing an opportunity to probe the molecular mechanism(s) of O2 sensing by ion channels (see e.g. Kemp et al., this volume). In addition, the consequences for cell function of hypoxic ion channel modulation are fairly well established. In most cases, an appropriate response to hypoxia (such as systemic vasodilation, pulmonary vasoconstriction or carotid body glomus cell transmitter release – see (Lopez-Barneo et al., 2001) for review) involves modulation of [Ca2+]i and this occurs primarily via modulation of Ca2+ influx (but in the lung vasculature this is contentious - see e.g. (Evans and Dipp, 2002)). Ca2+ influx can be regulated either through control of membrane potential via modulation of K+ channel activity (Buckler and Vaughan-Jones, 1994; Wyatt et al., 1995; Osipenko et al., 1997; Weir and Archer, 1998), or via a direct effect on Ca2+ channels (Franco- Obregon et al., 1995; Hool, 2001).

Item Type: Book Section
Date Type: Publication
Status: Published
Schools: Biosciences
Subjects: Q Science > QR Microbiology
Publisher: Kluwer
ISSN: 0065-2598
Last Modified: 04 Jun 2017 08:18

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