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Am J Physiol Heart Circ Physiol 281: H40-H47, 2001;
0363-6135/01 $5.00
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Vol. 281, Issue 1, H40-H47, July 2001

Inducible HSP70 mediates delayed cardioprotection via U-50488H pretreatment in rat ventricular myocytes

Jing-Jun Zhou1, Jian-Ming Pei1, Guan-Ying Wang1, Song Wu1, Wei-Ping Wang2, Chi-Hin Cho2, and Tak-Ming Wong1,3

Departments of 1 Physiology and 2 Pharmacology and 3 Institute of Cardiovascular Sciences and Medicine, Faculty of Medicine, University of Hong Kong, Hong Kong, China

To test the hypothesis that heat-shock proteins (HSPs) mediate delayed cardioprotection of prior kappa -opioid receptor (kappa -OR) stimulation, we first correlated cellular injury and viability with the expression of HSP70s in isolated rat ventricular myocytes subjected to prior kappa -OR stimulation with the selective agonist trans-(±)-3,4-dichloro-N-methyl-N-[2-(1-pyrrolidinyl)cyclohexyl]benzeneacetamide (U-50488H) and delayed lethal simulated ischemia (LSI). Cell injury and viability were indicated by lactate dehydrogenase release and trypan blue exclusion, respectively. The reduced injury and increased viability after pretreatment with U-50488H were concentration dependent and correlated directly with the expression of both stress-inducible (HSP70) and constitutive (HSC70) proteins. The effects mimic those with metabolic inhibition preconditioning (MIP). The cardioprotection against LSI by pretreatment with U-50488H and MIP was abolished and antagonized, respectively, via blockade of the kappa -OR by its selective antagonist, nor-binaltorphimine. We also found that blockade of the production of HSP70 but not HSC70 blocked the inhibitory effect of pretreatment with U-50488H on injury and viability. These observations provide evidence that stress-inducible HSP70 mediates delayed cardioprotection of prior kappa -OR stimulation.

kappa -opioid receptor; metabolic inhibition; preconditioning; heat shock protein 70; cellular injury


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