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Am J Physiol Heart Circ Physiol 283: H440-H447, 2002. First published March 28, 2002; doi:10.1152/ajpheart.00434.2001
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Vol. 283, Issue 1, H440-H447, July 2002

Opening of mitochondrial KATP channel occurs downstream of PKC-epsilon activation in the mechanism of preconditioning

Yoshito Ohnuma, Tetsuji Miura, Takayuki Miki, Masaya Tanno, Atsushi Kuno, Akihito Tsuchida, and Kazuaki Shimamoto

Second Department of Internal Medicine, Sapporo Medical University School of Medicine, Sapporo 060-8543, Japan

We examined whether the mitochondrial ATP-sensitive K channel (KATP) is an effector downstream of protein kinase C-epsilon (PKC-epsilon ) in the mechanism of preconditioning (PC) in isolated rabbit hearts. PC with two cycles of 5-min ischemia/5-min reperfusion before 30-min global ischemia reduced infarction from 50.3 ± 6.8% of the left ventricle to 20.3 ± 3.7%. PC significantly increased PKC-epsilon protein in the particulate fraction from 51 ± 4% of the total to 60 ± 4%, whereas no translocation was observed for PKC-delta and PKC-alpha . In mitochondria separated from the other particulate fractions, PC increased the PKC-epsilon level by 50%. Infusion of 5-hydroxydecanoate (5-HD), a mitochondrial KATP blocker, after PC abolished the cardioprotection of PC, whereas PKC-epsilon translocation by PC was not interfered with 5-HD. Diazoxide, a mitochondrial KATP opener, infused 10 min before ischemia limited infarct size to 5.2 ± 1.4%, but this agent neither translocated PKC-epsilon by itself nor accelerated PKC-epsilon translocation after ischemia. Together with the results of earlier studies showing mitochondrial KATP opening by PKC, the present results suggest that mitochondrial KATP-mediated cardioprotection occurs subsequent to PKC-epsilon activation by PC.

mitochondria; protein kinase C; infarct size


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