The aim of this study is to compare the role of nitric oxide (NO) system in realization of cardiogenic depressor reflexes in different animal species. Acute experiments were performed on anesthetized dogs and rats. Cardiogenic depressor reflex evoked by stimulation of cardiac receptors with veratrine (reproduction of the Bezold-Jarish reflex). Veratrine injections (5 μg, intracoronary and i.v.) resulted in a reflex decrease of mean arterial pressure and relaxation of coronary and peripheral vessels (1). Systemic inhibition of NOS by L-NNA (30 mg/kg, i.v.) significantly decreased the depressor reflex in the dogs but not in the rats. On the other hand inhibition of neuronal NOS by 7-nitroindazole (25 mg/kg, i.p.) decreased cardiogenic depressor reflex in the rats. We carried out the separate series experiment with NADPH-d staining to evaluate the distribution of NOS containing neurons in the medulla of dogs and rats. The main results of these experiments are: (i) the average number of NOS-containing neurons in the dorsomedial and ventrolateral medulla per section in dogs was larger than that in rats, while the density of the positive cells in the both regions in dogs was less than that in rats. (ii) Within the dorsal motor nucleus of vagus a lot of NOS-containing cells (preganglionic vagal neurons) were observed only in dog. Differences in the distribution of NO-generating neurons in the medullary cardiovascular centers and heterogeneity in the basal level of NO release may contribute to the peculiarities of the hemodynamic responses under formation cardiogenic reflexes in various species of animals. Thus NO-dependent mechanisms play an important role in realization of cardiogenic reflexes, predominantly related to n.vagus. These NO-dependent reflex reactions decrease cardiac afterload, therefore they could be admitted as compensatory reactions under cardiac pathology.