Ion Channel Regulation by AMPK The Route of Hypoxia-Response Coupling in the Carotid Body and Pulmonary Artery

A. Mark Evans; D. Grahame Hardie; Chris Peers; Christopher N. Wyatt; Benoit Viollet; Prem Kumar; Mark L. Dallas; Fiona Ross; Naoko Ikematsu; Heidi L. Jordan; Barbara L. Barr; J. Nicole Rafferty; Oluseye Ogunbayo

doi:10.1111/j.1749-6632.2009.05041.x

Ion Channel Regulation by AMPK The Route of Hypoxia-Response Coupling in the Carotid Body and Pulmonary Artery

A. Mark Evans, D. Grahame Hardie, Chris Peers, Christopher N. Wyatt, Benoit Viollet, Prem Kumar, Mark L. Dallas, Fiona Ross, Naoko Ikematsu, Heidi L. Jordan, Barbara L. Barr, J. Nicole Rafferty, Oluseye Ogunbayo

Deanery of Biomedical Sciences

Research output: Chapter in Book/Report/Conference proceeding › Chapter (peer-reviewed) › peer-review

Abstract

Vital homeostatic mechanisms monitor O-2 supply and adjust respiratory and circulatory function to meet demand. The pulmonary arteries and carotid bodies are key systems in this respect. Hypoxic pulmonary vasoconstriction (HPV) aids ventilation-perfusion matching in the lung by diverting blood flow from areas with an O-2 deficit to those rich in O-2, while a fall in arterial pO(2) increases sensory afferent discharge from the carotid body to elicit corrective changes in breathing patterns. We discuss here the new concept that hypoxia, by inhibiting oxidative phosphorylation, activates AMP-activated protein kinase (AMPK) leading to consequent phosphorylation of target proteins, such as ion channels, which initiate pulmonary artery constriction and carotid body activation. Consistent with this view, AMPK knockout mice exhibit an impaired ventilatory response to hypoxia. Thus, AMPK may be sufficient and necessary for hypoxia-response coupling and may regulate O-2 and thereby energy (ATP) supply at the whole body as well as the cellular level.

Original language	English
Title of host publication	Hypoxia and Consequences from Molecule to Malady
Editors	C. Peers, G. G. Haddad, N. S. Chandel
Place of Publication	OXFORD
Publisher	Blackwell Publishing Ltd
Pages	89-100
Number of pages	12
ISBN (Print)	978-1-57331-773-3
DOIs	https://doi.org/10.1111/j.1749-6632.2009.05041.x
Publication status	Published - 2009
Event	Conference on Hypoxia and Consequences - From Molecule to Malady - New York Duration: 12 Mar 2009 → 14 Mar 2009

Conference

Conference	Conference on Hypoxia and Consequences - From Molecule to Malady
City	New York
Period	12/03/09 → 14/03/09

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10.1111/j.1749-6632.2009.05041.x

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Evans, A. M., Hardie, D. G., Peers, C., Wyatt, C. N., Viollet, B., Kumar, P., Dallas, M. L., Ross, F., Ikematsu, N., Jordan, H. L., Barr, B. L., Rafferty, J. N., & Ogunbayo, O. (2009). Ion Channel Regulation by AMPK The Route of Hypoxia-Response Coupling in the Carotid Body and Pulmonary Artery. In C. Peers, G. G. Haddad, & N. S. Chandel (Eds.), Hypoxia and Consequences from Molecule to Malady (pp. 89-100). Blackwell Publishing Ltd. https://doi.org/10.1111/j.1749-6632.2009.05041.x

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title = "Ion Channel Regulation by AMPK The Route of Hypoxia-Response Coupling in the Carotid Body and Pulmonary Artery",

abstract = "Vital homeostatic mechanisms monitor O-2 supply and adjust respiratory and circulatory function to meet demand. The pulmonary arteries and carotid bodies are key systems in this respect. Hypoxic pulmonary vasoconstriction (HPV) aids ventilation-perfusion matching in the lung by diverting blood flow from areas with an O-2 deficit to those rich in O-2, while a fall in arterial pO(2) increases sensory afferent discharge from the carotid body to elicit corrective changes in breathing patterns. We discuss here the new concept that hypoxia, by inhibiting oxidative phosphorylation, activates AMP-activated protein kinase (AMPK) leading to consequent phosphorylation of target proteins, such as ion channels, which initiate pulmonary artery constriction and carotid body activation. Consistent with this view, AMPK knockout mice exhibit an impaired ventilatory response to hypoxia. Thus, AMPK may be sufficient and necessary for hypoxia-response coupling and may regulate O-2 and thereby energy (ATP) supply at the whole body as well as the cellular level.",

author = "Evans, {A. Mark} and Hardie, {D. Grahame} and Chris Peers and Wyatt, {Christopher N.} and Benoit Viollet and Prem Kumar and Dallas, {Mark L.} and Fiona Ross and Naoko Ikematsu and Jordan, {Heidi L.} and Barr, {Barbara L.} and Rafferty, {J. Nicole} and Oluseye Ogunbayo",

year = "2009",

doi = "10.1111/j.1749-6632.2009.05041.x",

language = "English",

isbn = "978-1-57331-773-3",

pages = "89--100",

editor = "C. Peers and Haddad, {G. G.} and Chandel, {N. S.}",

booktitle = "Hypoxia and Consequences from Molecule to Malady",

publisher = "Blackwell Publishing Ltd",

note = "Conference on Hypoxia and Consequences - From Molecule to Malady ; Conference date: 12-03-2009 Through 14-03-2009",

}

Evans, AM, Hardie, DG, Peers, C, Wyatt, CN, Viollet, B, Kumar, P, Dallas, ML, Ross, F, Ikematsu, N, Jordan, HL, Barr, BL, Rafferty, JN & Ogunbayo, O 2009, Ion Channel Regulation by AMPK The Route of Hypoxia-Response Coupling in the Carotid Body and Pulmonary Artery. in C Peers, GG Haddad & NS Chandel (eds), Hypoxia and Consequences from Molecule to Malady. Blackwell Publishing Ltd, OXFORD, pp. 89-100, Conference on Hypoxia and Consequences - From Molecule to Malady, New York, 12/03/09. https://doi.org/10.1111/j.1749-6632.2009.05041.x

Ion Channel Regulation by AMPK The Route of Hypoxia-Response Coupling in the Carotid Body and Pulmonary Artery. / Evans, A. Mark; Hardie, D. Grahame; Peers, Chris et al.
Hypoxia and Consequences from Molecule to Malady. ed. / C. Peers; G. G. Haddad; N. S. Chandel. OXFORD: Blackwell Publishing Ltd, 2009. p. 89-100.

Research output: Chapter in Book/Report/Conference proceeding › Chapter (peer-reviewed) › peer-review

TY - CHAP

T1 - Ion Channel Regulation by AMPK The Route of Hypoxia-Response Coupling in the Carotid Body and Pulmonary Artery

AU - Evans, A. Mark

AU - Hardie, D. Grahame

AU - Peers, Chris

AU - Wyatt, Christopher N.

AU - Viollet, Benoit

AU - Kumar, Prem

AU - Dallas, Mark L.

AU - Ross, Fiona

AU - Ikematsu, Naoko

AU - Jordan, Heidi L.

AU - Barr, Barbara L.

AU - Rafferty, J. Nicole

AU - Ogunbayo, Oluseye

PY - 2009

Y1 - 2009

N2 - Vital homeostatic mechanisms monitor O-2 supply and adjust respiratory and circulatory function to meet demand. The pulmonary arteries and carotid bodies are key systems in this respect. Hypoxic pulmonary vasoconstriction (HPV) aids ventilation-perfusion matching in the lung by diverting blood flow from areas with an O-2 deficit to those rich in O-2, while a fall in arterial pO(2) increases sensory afferent discharge from the carotid body to elicit corrective changes in breathing patterns. We discuss here the new concept that hypoxia, by inhibiting oxidative phosphorylation, activates AMP-activated protein kinase (AMPK) leading to consequent phosphorylation of target proteins, such as ion channels, which initiate pulmonary artery constriction and carotid body activation. Consistent with this view, AMPK knockout mice exhibit an impaired ventilatory response to hypoxia. Thus, AMPK may be sufficient and necessary for hypoxia-response coupling and may regulate O-2 and thereby energy (ATP) supply at the whole body as well as the cellular level.

AB - Vital homeostatic mechanisms monitor O-2 supply and adjust respiratory and circulatory function to meet demand. The pulmonary arteries and carotid bodies are key systems in this respect. Hypoxic pulmonary vasoconstriction (HPV) aids ventilation-perfusion matching in the lung by diverting blood flow from areas with an O-2 deficit to those rich in O-2, while a fall in arterial pO(2) increases sensory afferent discharge from the carotid body to elicit corrective changes in breathing patterns. We discuss here the new concept that hypoxia, by inhibiting oxidative phosphorylation, activates AMP-activated protein kinase (AMPK) leading to consequent phosphorylation of target proteins, such as ion channels, which initiate pulmonary artery constriction and carotid body activation. Consistent with this view, AMPK knockout mice exhibit an impaired ventilatory response to hypoxia. Thus, AMPK may be sufficient and necessary for hypoxia-response coupling and may regulate O-2 and thereby energy (ATP) supply at the whole body as well as the cellular level.

UR - http://www.scopus.com/inward/record.url?scp=70350365633&partnerID=8YFLogxK

U2 - 10.1111/j.1749-6632.2009.05041.x

DO - 10.1111/j.1749-6632.2009.05041.x

M3 - Chapter (peer-reviewed)

SN - 978-1-57331-773-3

SP - 89

EP - 100

BT - Hypoxia and Consequences from Molecule to Malady

A2 - Peers, C.

A2 - Haddad, G. G.

A2 - Chandel, N. S.

PB - Blackwell Publishing Ltd

CY - OXFORD

T2 - Conference on Hypoxia and Consequences - From Molecule to Malady

Y2 - 12 March 2009 through 14 March 2009

ER -

Ion Channel Regulation by AMPK The Route of Hypoxia-Response Coupling in the Carotid Body and Pulmonary Artery

Abstract

Conference

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