The role of nitric oxide (NO) in modulation of sensitivity ofmitochondnal permeability transition pore (MPTP) opening under exposure to calcium as inductor was studied in experiments on the isolated heart (on Langendorff) and isolated mitochondria. The MPTP opening was studied on the hearts under ischemia-reperfusion and of the mitochondrial calcium loading. We investigated the degree ofreperfusional injury of the heart functional state after preliminary administration of the classic inhibitor of MPTP opening: cyclosporin A, the nitroprussid sodium salt as NO donor, NO-synthase (NOS) inhibitors such as L-NMMA and aminoguanidin to perfusional solution, and also the influence of Ca+ in the range of concentrations (10(-8)-10(-4) M) on the mitochondrial swelling under its preincubation with L-NMMA (10(-4) M). It is shown that the protective effect of nitric oxide on myocardium under reperfusion of ischemic heart will be realised by means of the inhibiting of Ca2+ -induced MPTP opening.