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. Author manuscript; available in PMC: 2011 Dec 6.
Published in final edited form as: J Biol Chem. 2007 Aug 17;282(43):31366–31372. doi: 10.1074/jbc.M705268200

FIGURE 4. Summary of the myocardial-vascular metabolic signal transduction cascades initiated by phosphotransfer redistribution between adenylate kinase (AK) and creatine kinase (CK) governing the AMP/adenosine (Ado) cycle and the response of metabolic sensors (ATP-sensitive potassium channel, KATP, and AMP-activated protein kinase, AMPK).

FIGURE 4

Hypoxia or metabolic stress diminishes CK and increases AK flux, inducing AMP generation and subsequent AMP/adenosine signaling events. Adenosine/AMP signals delivered to vascular tissue through intercellular and para-cellular pathways induce signaling through adenosine receptors A(2A)AR, AMPKα1, and KATP channels. AMPKα1 activates eNOS, inducing NO/cGMP signaling, and could regulate KATP channels. Collectively, A(2A)AR, AMPKα1, eNOS, and KATP signaling converge on contractile protein, Ca2+, and membrane potential regulation, critical determinants of vascular tone.