AJP - Heart Track the topics, authors and articles important to you
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Heart Circ Physiol 288: H2412-H2421, 2005. First published January 6, 2005; doi:10.1152/ajpheart.00558.2004
0363-6135/05 $8.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
288/5/H2412    most recent
00558.2004v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in Web of Science
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 Web of Science (13)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Frederich, M.
Right arrow Articles by Balschi, J. A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Frederich, M.
Right arrow Articles by Balschi, J. A.

Hypoxia and AMP independently regulate AMP-activated protein kinase activity in heart

Markus Frederich,* Li Zhang,* and James A. Balschi

Nuclear Magnetic Resonance Laboratory for Physiological Chemistry, Division of Cardiovascular Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts

Submitted 9 June 2004 ; accepted in final form 30 December 2004

The hypothesis was tested that hypoxia increases AMP-activated protein kinase (AMPK) activity independently of AMP concentration ([AMP]) in heart. In isolated perfused rat hearts, cytosolic [AMP] was changed from 0.2 to 16 µM using metabolic inhibitors during both normal oxygenation (95% O2-5% CO2, normoxia) and limited oxygenation (95% N2-5% CO2, hypoxia). Total AMPK activity measured in vitro ranged from 2 to 40 pmol·min–1·mg protein–1 in normoxic hearts and from 5 to 55 pmol·min–1·mg protein–1 in hypoxic hearts. The dependence of the in vitro total AMPK activity on the in vivo cytosolic [AMP] was determined by fitting the measurements from individual hearts to a hyperbolic equation. The [AMP] resulting in half-maximal total AMPK activity (A0.5) was 3 ± 1 µM for hypoxic hearts and 28 ± 13 µM for normoxic hearts. The A0.5 for {alpha}2-isoform AMPK activity was 2 ± 1 µM for hypoxic hearts and 13 ± 8 µM for normoxic hearts. Total AMPK activity correlated with the phosphorylation of the Thr172 residue of the AMPK {alpha}-subunit. In potassium-arrested hearts perfused with variable O2 content, {alpha}-subunit Thr172 phosphorylation increased at O2 ≤ 21% even though [AMP] was <0.3 µM. Thus hypoxia or O2 ≤ 21% increased AMPK phosphorylation and activity independently of cytosolic [AMP]. The hypoxic increase in AMPK activity may result from either direct phosphorylation of Thr172 by an upstream kinase or reduction in the A0.5 for [AMP].

signal transduction; 31P-nuclear magnetic resonance spectroscopy; acetyl-CoA carboxylase


Address for reprint requests and other correspondence: J. A. Balschi, 221 Longwood Ave., BLI 247, Boston, MA 02115 (E-mail: jbalschi{at}rics.bwh.harvard.edu)




This article has been cited by other articles:


Home page
 Am. J. Physiol. Regul. Integr. Comp. Physiol.Home page
K.-O. Stenslokken, S. Ellefsen, J. A. W. Stecyk, M. B. Dahl, G. E. Nilsson, and J. Vaage
Differential regulation of AMP-activated kinase and AKT kinase in response to oxygen availability in crucian carp (Carassius carassius)
Am J Physiol Regulatory Integrative Comp Physiol, December 1, 2008; 295(6): R1803 - R1814.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
L. Zhang, H. He, and J. A. Balschi
Metformin and phenformin activate AMP-activated protein kinase in the heart by increasing cytosolic AMP concentration
Am J Physiol Heart Circ Physiol, July 1, 2007; 293(1): H457 - H466.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
K. Carvajal, E. Zarrinpashneh, O. Szarszoi, F. Joubert, Y. Athea, P. Mateo, B. Gillet, S. Vaulont, B. Viollet, X. Bigard, et al.
Dual cardiac contractile effects of the {alpha}2-AMPK deletion in low-flow ischemia and reperfusion
Am J Physiol Heart Circ Physiol, June 1, 2007; 292(6): H3136 - H3147.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
X.-H. Ning, S.-H. Chen, N. E. Buroker, C.-S. Xu, F.-R. Li, S.-P. Li, D.-S. Song, M. Ge, O. M. Hyyti, M. Zhang, et al.
Short-cycle hypoxia in the intact heart: hypoxia-inducible factor 1{alpha} signaling and the relationship to injury threshold
Am J Physiol Heart Circ Physiol, January 1, 2007; 292(1): H333 - H341.
[Abstract] [Full Text] [PDF]

Home page
 J. Physiol.Home page
J. R. B. Dyck and G. D. Lopaschuk
AMPK alterations in cardiac physiology and pathology: enemy or ally?
J. Physiol., July 1, 2006; 574(1): 95 - 112.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
L. Zhang, M. Frederich, H. He, and J. A. Balschi
Relationship between 5-aminoimidazole-4-carboxamide-ribotide and AMP-activated protein kinase activity in the perfused mouse heart
Am J Physiol Heart Circ Physiol, March 1, 2006; 290(3): H1235 - H1243.
[Abstract] [Full Text] [PDF]

Home page
 Mol. Cell. Biol.Home page
K. Terai, Y. Hiramoto, M. Masaki, S. Sugiyama, T. Kuroda, M. Hori, I. Kawase, and H. Hirota
AMP-Activated Protein Kinase Protects Cardiomyocytes against Hypoxic Injury through Attenuation of Endoplasmic Reticulum Stress
Mol. Cell. Biol., November 1, 2005; 25(21): 9554 - 9575.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online
Copyright © 2005 by the American Physiological Society.