Experimental Physiology Celebrating 100 years
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
QUICK SEARCH:   [advanced]


     

Physiology in Press

First published online on June 1, 2006.
Experimental Physiology (2006)
DOI: 10.1113/expphysiol.2006.033514
© The Physiological Society 2006
A more recent version of this article appeared on September 1, 2006
This Article
Right arrow Full Text (Rapid PDF)
Right arrow All Versions of this Article:
91/5/821    most recent
expphysiol.2006.033514v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Evans, A M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Evans, A M.

Received May 15, 2006
Revised May 19, 2006
Accepted after revision May 26, 2006

Respiratory [290]

AMP-activated protein kinase underpins hypoxic pulmonary vasoconstriction and carotid body excitation by hypoxia

A Mark Evans 1*

1 University of St Andrews

* To whom correspondence should be addressed. E-mail: ame3{at}st-andrews.ac.uk.


  Abstract
In order to maintain tissue pO2 within physiological limits, vital homeostatic mechanisms monitor O2 supply and respond to a fall in pO2 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 pO2 precipitates excitation-secretion coupling in carotid body type I cells, increased sensory afferent discharge from the carotid body and thereby elicits corrective changes in breathing patterns via the brain stem. There is a general consensus that hypoxia inhibits mitochondrial oxidative phosphorylation in these O2-sensing cells over a range of pO2 that has no such effect on other cell types. However, the question remains as to the identity of the mechanism that underpins thereafter 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.

Key Words: Carotid body, Hypoxia, Pulmonary artery




This article has been cited by other articles:


Home page
 Circ. Res.Home page
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]

Home page
 Exp PhysiolHome page
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]

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


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
Copyright © 2006 by the The Physiological Society.