Rats were given 1, 10, 40, or 100 ppm of vanadium in drinking water for seven months, while rabbits received 1 ppm of vanadium (as sodium metavanadate, NaVO3) in drinking water for twelve months. Rats developed arterial hypertension through complex effects of vanadium on central neurogenic pathways, central and periferal catecholaminergic mechanisms, specific autacoidal systems (kallikrein-kinin, reninangiotensin-aldosterone, enkephalin ones), and effectors (vessels and heart). The above effects of vanadium were in part confirmed in the rabbits which, however, did not show arterial hypertension since the increase of vascular resistance was counteracted by a reduction of both cardiac inotropism and cardiac output. Vanadium was accumulated in tissues as vanadyl; higher levels were found in the bone and in the kidney, but relevant amounts were determined in aorta, heart and brain. There was evidence, in the rabbits, that vanadium reduces synthesis and/or release of nitric oxide, the endothelium-derived vasodilating factor, likely through a reduced formation from bradykinin. The functional, analytical and morphological results obtained in this study show that chronic exposure to vanadium induces arterial hypertension by mechanisms only in part related to the levels and times of exposure, and to the species.