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NADPH oxidase does not account fully for O2-sensing in model airway chemoreceptor cells.

Abstract：

:A key feature of O2 sensing by chemoreceptor tissues is the hypoxic inhibition of K+ channels. However, mechanisms coupling a fall of pO2 to channel closure differ between tissues: O2 regulation of K+ channels in chemoreceptive neuroepithelial bodies and their immortal counterparts, H146 cells, involves altered reactive oxygen species generation by NADPH oxidase. In contrast, this enzyme complex is not involved in O2 sensing by the carotid body and pulmonary vasculature. Here, we provide pharmacological evidence to support a role for NADPH oxidase in hypoxic inhibition of K+ currents in H146 cells. Two structurally unrelated NADPH oxidase inhibitors, diphenylene iodonium and phenylarsine oxide, suppressed hypoxic inhibition of K+ currents recorded using the patch-clamp technique. Most importantly, however, neither inhibitor fully blocked this response. Our findings provide the first evidence that multiple mechanisms may coexist within a specific cell type to account for hypoxic suppression of K+ channel activity.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

O'Kelly I,Peers C,Kemp PJ

doi

10.1006/bbrc.2001.4919

subject

Has Abstract

pub_date

2001-05-25 00:00:00

pages

1131-4

issue

5

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(01)94919-8

journal_volume

283

pub_type

杂志文章

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