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Acute Hypoxic Regulation of Recombinant THIK-1...
Journal article

Acute Hypoxic Regulation of Recombinant THIK-1 Stably Expressed in HEK293 Cells

Abstract

Hypoxic inhibition of O2-sensitive K+ channels plays a key role in mediating numerous cellular responses which counteract the deleterious effects of hypoxia. In type I cells of the carotid body (CB), a neurosecretory organ that responds to hypoxia by releasing neurotransmitters from specialized O2-sensing type I cells onto sensory nerve endings, hypoxic inhibition of K+ channels underlies the membrane depolarisation (Lopez-Barneo et al., 1988) that stimulates Ca2+ entry and neurotransmitter release (Urena et al., 1994). In other neurosecretory cells, such as those located in the neuroepithelial cell bodies of the lung (Youngson et al., 1993) and the adrenal medulla (Thompson and Nurse, 1998), hypoxic inhibition of K+ channels provides a critical link between O2 levels and the appropriate cellular responses.

Authors

FEARON IM; CAMPANUCCI VA; BROWN ST; HUDASEK K; O’KELLY IM; NURSE CA

Journal

Advances in Experimental Medicine and Biology, Vol. 580, , pp. 203–208

Publisher

Springer Nature

Publication Date

January 1, 2006

DOI

10.1007/0-387-31311-7_31

ISSN

0065-2598
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