Brief periods of ischaemia increase the myocardial resistance against a subsequent and more severe ischaemia. In this “ischaemic pre-conditioning” (IPC), articulated in two phases, a pivotal mechanism resides in the activation of cardiac mitochondrial ATP-sensitive potassium channels (mitoKATP). Therefore, mitoKATP-openers can mimic the IPC and can induce a “pharmacological pre-conditioning” against the myocardial damage due to ischaemic episodes. In particular, those molecules endowed of selectivity towards the mitoKATP channels have been proposed as anti-ischaemic cardioprotective drugs, devoid of other significant side-effects (such as negative inotropic activity, hypotension or hyperglycemia) linked to the opening of sarcolemmal KATP channels. In this paper, the experimental observation accounting for the relevant role of mitoKATP channels in IPC, the mechanisms involved and some representative molecules acting as mitoKATP-activators are reported.
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