Objective: It is well known that dinitrosyl iron complexes (DNIC) play essential role, as physiological NO forms in mammalian organism. The injection of this substance exerts prolonged hypotensive action. The aim of the present research was study of DNIC with glutathione ligand (DNIC-GH) action in rat organism in different physiological states. Design and method: The experiments were carried out on normotensive and hypertensive rats. Standard doses of DNIC were injected into rats by intravenous, intraperitoneal, intramuscular, subcutaneous injections, and rectal introduction. Most experiments were carried out on the rats in native physiological conditions, while the others were performed on the model of regional cardiac ischemia, or during general endotoxic shock. In all experiments registration of mean aortic pressure and heart rate were carried out, and DNIC concentrations in whole blood and organs were obtained by EPR method. DNIC-GH effect on NO levels was studied using spin traps. Results: It has been shown that DNIC injection exerted substantial and prolonged hypotensive effect on normotensive and hypertensive rats. The hypotensive action of DNIC and its accumulation in whole blood and mammalian organs depended on the mode of introduction of this substance, and the most substantial and prolonged effects were registered after intravenous and subcutaneous injections. We have shown that DNIC-GH in organism operated mostly, as potent origin of NO physiological forms, such as DNIC with protein ligands and S-nitrosothiols, and its effect on free NO level was substantially slower. Meantime, DNIC-GH molecules also exerted protective action under the condition of NO hyperproduction. In particular, on the model of regional myocardial ischemia DNIC-GH injection resulted in cardioprotective action by suppression of free NO hyperproduction in ischemic area and effective scavenging of toxic oxygen active species. In the other experiments, DNIC-GH injection also exerted cytoprotective effect, causing the suppression of NO hyperproduction in rat lung and liver during endotoxing shock. Conclusions: DNIC-GH molecules in organism act generally, as the origin of NO physiological forms which cause prolonged hypotensive action. Meantime, this substance exerts regulating effect on NO level, suppressing its hyperproduction in organs.