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Department of Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee, Wisconsin 53226
We
examined the role of the sarcolemmal and mitochondrial KATP
channels in a rat model of ischemic preconditioning (IPC). Infarct size
was expressed as a percentage of the area at risk (IS/AAR). IPC
significantly reduced infarct size (7 ± 1%) versus control (56 ± 1%). The sarcolemmal KATP channel-selective antagonist HMR-1098 administered before IPC did not significantly attenuate cardioprotection. However, pretreatment with the mitochondrial KATP channel-selective antagonist 5-hydroxydecanoic acid
(5-HD) 5 min before IPC partially abolished cardioprotection (40 ± 1%). Diazoxide (10 mg/kg iv) also reduced IS/AAR (36.2 ± 4.8%), but this effect was abolished by 5-HD. As an index of
mitochondrial bioenergetic function, the rate of ATP synthesis in the
AAR was examined. Untreated animals synthesized ATP at 2.12 ± 0.30 µmol · min
1 · mg
mitochondrial protein1. Rats subjected to
ischemia-reperfusion synthesized ATP at 0.67 ± 0.06 µmol · min1 · mg
mitochondrial protein1. IPC significantly increased
ATP synthesis to 1.86 ± 0.23 µmol · min1 · mg
mitochondrial protein1. However, when 5-HD was
administered before IPC, the preservation of ATP synthesis was
attenuated (1.18 ± 0.15 µmol · min1 · mg
mitochondrial protein1). These data are consistent
with the notion that inhibition of mitochondrial KATP
channels attenuates IPC by reducing IPC-induced protection of
mitochondrial function.
5-hydroxydecanoic acid; HMR-1098; adenosine 5'-diphosphate-sensitive potassium channel; mitochondria
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