In normotensive rats (NTR) and spontaneously hypertensive rats (SHR) with high (subgroup 1) and low (subgroup 2) level of the systemic arterial presure (SAP) we studied an activity of arginase and nitric oxide synthase (NOS) in different tissues, and the content of their metabolites: urea and nitrit anion (NO₂ ^-). In isolated preparations of a thoracic aorta we recorded endothelium-dependent (ED) dilator reactions on acetylcholine (Ach). It has been found that in heart, aorta, plasma and erythrocytes of rats (subgroup 2) both the activity of arginase and content of urea increase remarkably. In heart, the activity of arginase reaches 27,96 ± 5,92 nmol ? min^-1 ? mg^-1 of protein, in aorta 4,74 ± 0,99 nmol ? min?1 ? mg?1 of protein (as compared with NTR 1,32 ± 0,12 nmol ? min^-1 ? mg^-1 of protein and 1,12 ± 0,07 nmol ? min?1 ? mg?1 of protein, accordingly). Content of urea in heart reaches 679,5 ± 121,19 nmol ? mg?1 of protein, in aorta 350,6 ± 63,6 nmol ? mg^-1 of protein (in NTR it was 36,8 ± 5,3 nmol ? mg^-1 of protein and 43,02 ± ± 9,55 nmol ? min^-1 ? mg^-1 of protein, accordingly). It was followed with a decrease in the NOS activity and heterogenous changes in NO2 ? content in the tissues under exploration. For example, the activity of NOS in heart and aorta decreased to 0,018 ± 0,005 nmol ? min^-1? mg^-1 of protein, in aorta 0,183 ± 0,037 nmol ? min^-1? mg^-1 of protein, accordingly, as compared to 0,093±0,014 nmol ? min^-1 ? mg^-1 of protein and 0,41±0,07 nmol ? min^-1 ? mg^-1 of protein in NTR. Content of NO2 ? in aorta decreased by 0,79 ± 0,06 nmol ? mg-1of protein, but in heart it increased to 0,63 ± ± 0,13 nmol ? mg^-1 of protein, (in NTR it was 2,15 ± 0,18 nmol ? mg^-1of protein and 0264 ± 0,04 nmol ? min^-1 ? mg^-1of protein, accordingly). In rats, subgroup 2, ED dilator responses of the smooth muscle (SM) of the thoracic aorta were inhibited by Ach (10?6 mol). Their amplitude reduced by almost twice, and a latency for their response became 4 times as much. All the changes in the biochemical parametres in heart, aorta, plasma and erythrocytes, and changes in contractile activity of vascular SM proved to be also characteristic for rats in subgroup 1, but they were less expreassed quantitatively. Thus, for the first time we have studied an activity of two alternative pathways for the metabolism of L-arginine on the model of arterial hypertension. The data obtained evidence that at hypertension non-oxidative (arginase) pathway of L-arginine metabolism is activated, while the oxidative pathway (NOS) is inhibited. Changes in the balance between them are followed with an essential inhibition of ED vasodilator responses. All this give us the prove to think of the origin for the arterial pressure increase to be both genetically and quantitatively determined damages in the biochemical homeostasis and dependent on it endothelial regulation of vascular tone.