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The mitochondrial Ca(2+)-activated K(+) channel contributes to cardioprotection by limb remote ischemic
Yang Cao1, Shi-zhong Zhang, Shu-Qin Zhao
1Department of Physiology, Medical Science College of China Three Gorges University, Yichang, China.
Aims:
To investigate the role of the mitochondrial Ca(2+)-activated K(+) channel in cardioprotection induced by limb remote ischemic preconditioning.
Main Methods:
Male Sprague-Dawley rats (250-300 g) were randomized into control, ischemia/reperfusion (I/R), remote ischemic preconditioning (RPC), NS1619 (a specific mitochondrial Ca(2+)-activated K(+) channel opener), and RPC+paxilline (a specific mitochondrial Ca(2+)-activated K(+) channel inhibitor) groups. RPC was induced by 4 cycles of 5 min of ligation followed by 5 min of reperfusion of the left femoral artery. Myocardial I/R was achieved by ligation of the left anterior descending coronary artery for 30 min, followed by 120 min of reperfusion. Infarct size was determined by 2,3,5-triphenyltetrazolium chloride staining, the hemodynamics were monitored, and lactate dehydrogenase (LDH) levels in the coronary effluent, manganese superoxide dismutase (Mn-SOD) content in mitochondria and mitochondrial membrane potential were measured spectrophotometrically. The ultrastructure of cardiomyocyte mitochondria was assessed by electron microscopy.
Key Findings:
NS1619 (10 μM) improved heart function, decreased infarct size, reduced LDH release, maintained mitochondrial structural integrity and mitochondrial membrane potential, and increased the mitochondrial content of Mn-SOD to the same degree as RPC treatment. However, paxilline (1 μM) eliminated the cardioprotective effect conferred by RPC.
Significance:
The mitochondrial Ca(2+)-activated K(+) channel participates in the myocardial protection by limb remote ischemic preconditioning.
