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First published online on July 20, 2006.
Experimental Physiology (2006)
DOI: 10.1113/expphysiol.2006.034587
© The Physiological Society 2006
A more recent version of this article appeared on September 1, 2006
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Received May 26, 2006
Revised June 19, 2006
Accepted after revision July 10, 2006

Respiratory [290]

Detecting acute changes in oxygen: will the real sensor please stand up?

Paul J Kemp 1*

1 Cardiff University

* To whom correspondence should be addressed. E-mail: kemppj{at}cf.ac.uk.


  Abstract
The majority of physiological processes proceed most favourably when O2 is in plentiful supply. However, there are a number of physiological and pathological circumstances where this supply is reduced either acutely or chronically. A crucial homeostatic response to such arterial hypoxaemia is carotid body excitation and a resultant increase in ventilation. Central to this response in carotid body, and many other chemosensory tissues, is the rapid inhibition of ion channels by hypoxia. Since the first direct demonstration of hypoxia-evoked depression in K+ channel activity, the number of mechanisms which have been proposed to serve as the primary O2 sensor have been almost as numerous as the experimental strategies with which to probe their nature. Three of the current favourite candidate mechanisms are mitochondria, AMP-activated kinase and hemeoxygenase 2; a fourth proposal has been NADPH oxidase, but recent evidence suggests that this enzyme plays a secondary role in the O2 sensing process. All of these proposals have attractive points, but none can fully reconcile all of the data which have accumulated over the last two decades or so, suggesting that there may, in fact, not be an unique sensing system even within a single cell-type. This latter point is key, because it implies that the ability of a cell to respond appropriately to decreased O2 availability is biologically so important that several mechanisms have evolved to ensure that cellular function is never compromised during moderate to severe hypoxic insult.

Key Words: Hypoxia, Potassium channel, Respiratory control




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