The University of Southampton
University of Southampton Institutional Repository
Warning ePrints Soton is experiencing an issue with some file downloads not being available. We are working hard to fix this. Please bear with us.

Airway chemotransduction: from oxygen sensor to cellular effector

Airway chemotransduction: from oxygen sensor to cellular effector
Airway chemotransduction: from oxygen sensor to cellular effector
The process of sensing, transducing, and acting on environmental cues is critical to normal physiologic function. Furthermore, dysfunction of this process can lead to the development of disease. This is especially true of the homeostatic mechanisms that have evolved to maintain the carriage of O2 to respiring tissues during acute hypoxic challenge. During periods of reduced O2 availability, three major mechanisms act conjointly to increase ventilation and optimize the ventilation-perfusion ratio throughout the lung by directing pulmonary blood flow to better ventilated areas of the lung. These mechanisms are as follows: (1) increased carotid sinus nerve discharge rate to the respiratory centers of the brain, (2) intrinsic hypoxic vasoconstriction of pulmonary resistance vessels, and (3) potential local and central modulation via stimulation of neuroepithelial bodies of the lung. The key to the rapid response to the O2 signal is the ability of each of these tissues to sense acutely the changes in PO2, to transduce the signal, and for cellular effectors to initiate compensatory mechanisms that will offset rapidly the reduction in PO2 before O2 availability to tissues is compromised. This review concentrates on the signal transduction mechanism that links altered PO2 to depolarization in the recently proposed airway chemosensory element, the neuroepithelial body (and its immortalized cellular counterpart, the H146 cell line), and discusses the pertinent similarities and differences that exist between airway, carotid body, and pulmonary arteriolar O2 sensing.
cues, tandem pore domain, cell line, physiology, respiratory mucosa, blood, oxygen, research support, research, potassium channels, anoxia
1073-449X
S17-S24
Kemp, Paul J.
c982082a-81d9-404a-b2e6-f2eb19cd1163
Lewis, Anthony
2e8de8fb-88fa-45cf-b660-80977fdb4966
Hartness, Matthew E.
02b71674-0f93-472d-92f4-c385c32b6e2d
Searle, Gavin J.
4ea8d469-6990-41fc-bfc0-e866b5408457
Miller, Paula
855653d0-8dc1-4694-b4fe-d2482ab2f318
O'Kelly, Ita
25d4a504-705e-42ca-9add-853845f0b4a6
Peers, Chris
da7f1f51-8685-46be-bf46-f43c519a3579
Kemp, Paul J.
c982082a-81d9-404a-b2e6-f2eb19cd1163
Lewis, Anthony
2e8de8fb-88fa-45cf-b660-80977fdb4966
Hartness, Matthew E.
02b71674-0f93-472d-92f4-c385c32b6e2d
Searle, Gavin J.
4ea8d469-6990-41fc-bfc0-e866b5408457
Miller, Paula
855653d0-8dc1-4694-b4fe-d2482ab2f318
O'Kelly, Ita
25d4a504-705e-42ca-9add-853845f0b4a6
Peers, Chris
da7f1f51-8685-46be-bf46-f43c519a3579

Kemp, Paul J., Lewis, Anthony, Hartness, Matthew E., Searle, Gavin J., Miller, Paula, O'Kelly, Ita and Peers, Chris (2002) Airway chemotransduction: from oxygen sensor to cellular effector. American Journal of Respiratory and Critical Care Medicine, 166 (12 Suppl: Oxida), S17-S24. (doi:10.1164/rccm.2206009).

Record type: Article

Abstract

The process of sensing, transducing, and acting on environmental cues is critical to normal physiologic function. Furthermore, dysfunction of this process can lead to the development of disease. This is especially true of the homeostatic mechanisms that have evolved to maintain the carriage of O2 to respiring tissues during acute hypoxic challenge. During periods of reduced O2 availability, three major mechanisms act conjointly to increase ventilation and optimize the ventilation-perfusion ratio throughout the lung by directing pulmonary blood flow to better ventilated areas of the lung. These mechanisms are as follows: (1) increased carotid sinus nerve discharge rate to the respiratory centers of the brain, (2) intrinsic hypoxic vasoconstriction of pulmonary resistance vessels, and (3) potential local and central modulation via stimulation of neuroepithelial bodies of the lung. The key to the rapid response to the O2 signal is the ability of each of these tissues to sense acutely the changes in PO2, to transduce the signal, and for cellular effectors to initiate compensatory mechanisms that will offset rapidly the reduction in PO2 before O2 availability to tissues is compromised. This review concentrates on the signal transduction mechanism that links altered PO2 to depolarization in the recently proposed airway chemosensory element, the neuroepithelial body (and its immortalized cellular counterpart, the H146 cell line), and discusses the pertinent similarities and differences that exist between airway, carotid body, and pulmonary arteriolar O2 sensing.

This record has no associated files available for download.

More information

Published date: 7 October 2002
Keywords: cues, tandem pore domain, cell line, physiology, respiratory mucosa, blood, oxygen, research support, research, potassium channels, anoxia

Identifiers

Local EPrints ID: 59925
URI: http://eprints.soton.ac.uk/id/eprint/59925
ISSN: 1073-449X
PURE UUID: ab9661a4-df31-4881-a82c-b488fe593e36

Catalogue record

Date deposited: 05 Sep 2008
Last modified: 08 Jan 2022 04:03

Export record

Altmetrics

Contributors

Author: Paul J. Kemp
Author: Anthony Lewis
Author: Matthew E. Hartness
Author: Gavin J. Searle
Author: Paula Miller
Author: Ita O'Kelly
Author: Chris Peers

Download statistics

Downloads from ePrints over the past year. Other digital versions may also be available to download e.g. from the publisher's website.

View more statistics

Atom RSS 1.0 RSS 2.0

Contact ePrints Soton: eprints@soton.ac.uk

ePrints Soton supports OAI 2.0 with a base URL of http://eprints.soton.ac.uk/cgi/oai2

This repository has been built using EPrints software, developed at the University of Southampton, but available to everyone to use.

We use cookies to ensure that we give you the best experience on our website. If you continue without changing your settings, we will assume that you are happy to receive cookies on the University of Southampton website.

×