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Am J Physiol Heart Circ Physiol 288: H2412-H2421, 2005. First published January 6, 2005; doi:10.1152/ajpheart.00558.2004
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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)




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