The effects of non-enzymatic disintegration of SIN-1 products (nitric oxide, superoxide anion and peroxynitrite) on Ca(2+)-transport of sarcoplasmic reticulum were studied on homogenates of rats myocardium. It was shown that SIN-1 (30 microM) exerts a significant activating effect on ryanodine-sensitive calcium channels resulted in three-fold increase of Ca2+ release rate via these channels. Such effect of SIN-1 realized mainly by nitric oxide effect and, partially, superoxide radical. SIN-1 did not effect the Ca(2+)-ATPase activity of sarcoplasmic reticulum.
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