Objective: To examine the direct vasodilating effect of viper poison on isolated rat aortic rings as well as preservation of rat aortic vascular function after incubation with 150μg/Lof viper poison. Materials and methods: Viper venom was made in the laboratory for the primary treatment of snake venoms within the Institute of Immunology in Zagreb.The samples which were used in the experiments, were a series production viper venom called KrKa. The production series of toxins were in crystalline form, stored in a dark bottle and kept in a dark, cool place (4°C) until its further use. For our research the viper venom sample, Krka series, was characterized biochemically and biologically standardized, after which we examined its effect on the model of isolated rat aortic vascular rings. The poison was kept in crystalline form, and just before the experiments on isolated rat aorta, melted in a modified Krebs-Henseleit solution. For research purposes we used ten Sprague Dawley strain rats; males, 3-6 months old, weighing 300-500 g, bred in the University residences for experimental animals in Split. All procedures conducted in the study were approved by the Ethics Committee for Biomedical Research, School of Medicine in Split. Results: Viper venom showed a direct vasodilating effect on noradrenaline precontracted rat aorta with an intact endothelium. On the vascular rings without endotheliumvasodilating effect of viper venom was also accomplished. Maximum vasodilating effect of venom was achieved at the highest dose (150μg/L) and was significantly greater in rings with endothelium compared to rings without endothelium. Viper venom used in the highest concentration significantly impaired the contractile response of rat aorta to noradrenaline. Incubation of intact aortic rings with venom significantly shifts the curve of thenoradrenaline concentration - the vasoconstricting effect to the right. Endothelium-dependent vasodilatation response to acetylcholine of the aorta was significantly reduced after administration of venom. Incubation with venom moves the curve of concentration of acetylcholine - a vasodilating effect to the right, and significantly reduces the maximum vasodilatory effect. The concentration of norepinephrine and acetylcholine, that is necessary to achieve 50% of their maximal effect was lower in intact aortic rings in relation to the rings incubated with venom. Conclusion: Biochemically characterized and biologically standardized viper venom causes a dose-dependent effect on isolated rat aortic rings. Viper venom showed a direct vasodilating effect on previously contracted aorta with endothelium and without endothelium. Vasodilating effect of poison is only partially dependent on the endothelium and significantly impairs the norepinephrine-induced contractile response of rat aorta. Endothelium-dependent vasodilatation of the aorta in response to acetylcholinewas significantly reduced after administration of poison. Viper venom significantly impairs contractile and vasodilatory function in a model of isolated vascular rings.