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Potassium channel openers and the expression of BCL-type proteins in cardiac myocytes

Cardiovascular disease is a leading cause of death worldwide. In recent years it has emerged that a major contributory to the development of the disease is the dysfunction of cardiomyocytes. It is now believed that cardiomyocytes die not only by necrosis but also by apoptosis. Apoptosis is a process controlled by a variety of signals, including proteins of the bcl-2 family. In 1991, the mitochondrial ATP regulated potassium channel (mitoK ATP channel) was identified in the inner membrane of heart mitochondria [Inoue et al., Nature 352 (1991) 244]. Like plasma membrane channels, the mitochondrial channel is inhibited by antidiabetic sulfonylureas and activated by potassium channel openers (KCOs). Importantly, in cardiac muscle, the mitoK ATP channel was found to play an important role in the protection of cardiomyocytes against ischemia/reperfusion injury. The activation of the mitoK ATP channel by KCO-diazoxide seems to mimic ischemic preconditioning in heart muscle. Cardioprotective action of mitochondrial KCOs probably involves multiple mechanisms, including effects on cellular apoptosis. In this study, we analysed the effects of oxidative stress on neonatal rat cardiac ventricular myocytes. We and others [Akao et al., Circ. Res. 88 (2001) 1267] observed that 100 µM diazoxide protects these cells against death induced by 100 µM hydrogen peroxide. Moreover, diazoxide prevents hydrogen peroxide induced mitochondrial potential depolarization (measured with the fluorescent probe JC-1). In our study, we also aim to describe the expression changes of the pro-and anti-apoptotic proteins in the presence of diazoxide. This will include bax, bcl-2, and bcl-x L both at the mRNA and the protein level.