HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 91/5/821    most recent expphysiol.2006.033514v1 Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Evans, A. M. Search for Related Content PubMed PubMed Citation Articles by Evans, A. M. Related Collections Respiratory

¹ Division of Biomedical Sciences, School of Biology, Bute Building, University of St Andrews, St Andrews, Fife KY16 9TS, UK

Abstract

In order to maintain tissue partial pressure of oxygen (P_O2) within physiological limits, vital homeostatic mechanisms monitor O₂ supply and respond to a fall in P_O2 by altering respiratory and circulatory function, and the capacity of the blood to transport O₂. Two systems that are key to this process in the acute phase are the pulmonary arteries and the carotid bodies. Hypoxic pulmonary vasoconstriction is driven by mechanisms intrinsic to the pulmonary arterial smooth muscle and endothelial cells, and aids ventilation–perfusion matching in the lung by diverting blood flow from areas with an O₂ deficit to those that are rich in O₂. By contrast, a fall in arterial P_O2 precipitates excitation–secretion coupling in carotid body type I cells, increases sensory afferent discharge from the carotid body and thereby elicits corrective changes in breathing patterns via the brainstem. There is a general consensus that hypoxia inhibits mitochondrial oxidative phosphorylation in these O₂-sensing cells over a range of P_O2 values that has no such effect on other cell types. However, the question remains as to the identity of the mechanism that underpins hypoxia–response coupling in O₂-sensing cells. Here, I lay out the case in support of a primary role for AMP-activated protein kinase in mediating chemotransduction by hypoxia.

(Received 15 May 2006; accepted after revision 26 May 2006; first published online 1 June 2006)
Corresponding author A. M. Evans: Division of Biomedical Sciences, School of Biology, Bute Building, University of St Andrews, St Andrews, Fife KY16 9TS, UK. Email: ame3{at}st-andrews.ac.uk

This article has been cited by other articles:

				N. Weissmann Nitric Oxide-Mediated Zinc Release: A New (Modulatory) Pathway in Hypoxic Pulmonary Vasoconstriction Circ. Res., June 20, 2008; 102(12): 1451 - 1454. [Full Text] [PDF]

				J. P. T. Ward Curiouser and curiouser: the perplexing conundrum of reactive oxygen species and hypoxic pulmonary vasoconstriction Exp Physiol, September 1, 2007; 92(5): 819 - 820. [Full Text] [PDF]

				N. R. Prabhakar Novel partners and mechanisms in oxygen sensing Exp Physiol, September 1, 2006; 91(5): 801 - 801. [Full Text] [PDF]