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Cardioprotective effects of stretch are mediated by activation of sarcolemmal, not mitochondrial, ATP-sensitive potassium channels

Centro de Investigaciones Cardiovasculares, Universidad Nacional de La Plata, La Plata, Buenos Aires, Argentina

Submitted 15 January 2007 ; accepted in final form 26 March 2007

To determine whether sarcolemmal and/or mitochondrial ATP-sensitive potassium (K_ATP) channels (sarcK_ATP, mitoK_ATP) are involved in stretch-induced protection, isolated isovolumic rat hearts were assigned to the following protocols: nonstretched hearts were subjected to 20 min of global ischemia (Is) and 30 min of reperfusion, and before Is stretched hearts received 5 min of stretch + 10 min of no intervention. Stretch was induced by a transient increase in left ventricular end-diastolic pressure (LVEDP) from 10 to 40 mmHg. Other hearts received 5-hydroxydecanoate (5-HD; 100 µM), a selective inhibitor of mitoK_ATP, or HMR-1098 (20 µM), a selective inhibitor of sarcK_ATP, before the stretch protocol. Systolic function was assessed through left ventricular developed pressure (LVDP) and maximal rise in velocity of left ventricular pressure (+dP/dt_max) and diastolic function through maximal decrease in velocity of left ventricular pressure (–dP/dt_max) and LVEDP. Lactate dehydrogenase (LDH) release and ATP content were also measured. Stretch resulted in a significant increase of postischemic recovery and attenuation of diastolic stiffness. At 30 min of reperfusion LVDP and +dP/dt_max were 87 ± 4% and 92 ± 6% and –dP/dt_max and LVEDP were 95 ± 9% and 10 ± 4 mmHg vs. 57 ± 6%, 53 ± 6%, 57 ± 10%, and 28 ± 5 mmHg, respectively, in nonstretched hearts. Stretch increased ATP content and did not produce LDH release. 5-HD did not modify and HMR-1098 prevented the protection achieved by stretch. Our results show that the beneficial effects of stretch on postischemic myocardial dysfunction, cellular damage, and energetic state involve the participation of sarcK_ATP but not mitoK_ATP.

ischemia; reperfusion