Abstract
The effect of pinacidil was studied on calcium-loaded rat heart mitochondria (RHM) in the presence of succinate and rotenone. In experiments with pinacidil, the swelling of these mitochondria increased in media with NH4NO3 or K-acetate, but the inner membrane potential (ΔΨmito) and the respiration in 3 or 2,4-dinitrophenol-stimulated states of these organelles decreased due to the opening of the mitochondrial permeability transition pore (MPTP) in their inner membrane. These effects were inhibited by cyclosporin A and ADP. It was concluded that the protective effect of pinacidil in the cardiac muscle under ischemia/reperfusion may be associated with both the stimulation of mitochondrial swelling and a decrease in RHM calcium overload resulted in ΔΨmito fall due to mild uncoupling effect of pinacidil.
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