The influence of the donor and the precursor of NO, namely 100 mM sodium nitroprusside and sodium nitrite on the energo-dependent Ca(2+)-transport in isolated mitochondria from rat myometrium was investigated. Changes in the mitochondrial matrix Ca(2+)-concentration was evaluated by spectrofluorimetry using Ca2+ sensitive probe Fluo-4 AM. Mg(2+)-ATP-dependent Ca(2+)-accumulation on mitochondria in the presence of succinate significantly stimulated by nitric oxide, in particular, 100 microM sodium nitroprusside amplified the transport by 1.6 times relative to its control values. NO effect becomes significant only when the incubation of mitochondria with the compounds was performed. Ca(2+)-accumulation in the presence of sodium nitroprusside effectively suppressed by protonophore (CCCP) and ruthenium red (10 microM). It was concluded that inner mitochondrial membrane Ca(2+)-uniporter stimulated by nitrogen oxide. Ca(2+)-accumulation in mitochondria in the presence of sodium nitroprusside was not sensitive to the action of a specific permeability transition pore inhibitor cyclosporine (5 microM). This data indicates that the role of permeability transition pore is less significant than Ca(2+)-uniporter in the processes of Ca(2+)-transport in mitochondria under the nitric oxide action. Thus, nitric oxide stimulates the energo-dependent Ca(2+)-accumulation by myometrium mitochondria mediated their inner membrane Ca(2+)-uniporter functioning.