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Cardioprotection through a PKC-dependent decrease in myofilament ATPase

Department of Physiology, University of Tennessee, Memphis, Tennessee 38163

Submitted 24 January 2003 ; accepted in final form 21 May 2003

Activation of myocardial -opioid receptor-protein kinase C (PKC) pathways may improve postischemic contractile function through a myofilament reduction in ATP utilization. To test this, we first examined the effects of PKC inhibitors on -opioid receptor-dependent cardioprotection. The -opioid receptor agonist U50,488H (U50) increased postischemic left ventricular developed pressure and reduced postischemic end-diastolic pressure compared with controls. PKC inhibitors abolished the cardioprotective effects of U50. To determine whether -opioid-PKC-dependent decreases in Ca²⁺-dependent actomyosin Mg²⁺-ATPase could account for cardioprotection, we subjected hearts to three separate actomyosin ATPase-lowering protocols. We observed that moderate decreases in myofibrillar ATPase were equally cardioprotective as -opioid receptor stimulation. Immunoblot analysis and confocal microscopy revealed a -opioid-induced increase in myofilament-associated PKC-, and myofibrillar Ca²⁺-independent PKC activity was increased after -opioid stimulation. This PKC-myofilament association led to an increase in troponin I and C-protein phosphorylation. Thus we propose PKC- activation and translocation to the myofilaments causes a decrease in actomyosin ATPase, which contributes to the -opioid receptor-dependent cardioprotective mechanism.

U50,488H; Western blot; confocal microscopy; protein kinase C activity; left ventricular developed pressure; -opioid

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