Carmignani M, Volpe A R, Boscolo P, Ripanti G, Giuliano G
Dept. of Basic and Applied Biology, University of L'Aquila, Coppito (AQ), Italy.
G Ital Med Lav. 1995 Jan-Nov;17(1-6):51-9.
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.
给大鼠饮用含1、10、40或100 ppm钒的水，持续七个月，而给兔子饮用含1 ppm钒（以偏钒酸钠，NaVO₃形式）的水，持续十二个月。钒通过对中枢神经源性途径、中枢和外周儿茶酚胺能机制、特定的自身活性物质系统（激肽释放酶 - 激肽、肾素 - 血管紧张素 - 醛固酮、脑啡肽系统）以及效应器（血管和心脏）的复杂作用，使大鼠患上动脉高血压。钒的上述作用在兔子身上部分得到证实，然而，兔子并未出现动脉高血压，因为血管阻力的增加被心肌收缩力和心输出量的降低所抵消。钒以氧钒根形式在组织中蓄积；在骨骼和肾脏中发现含量较高，但在主动脉、心脏和大脑中也测定到了相当数量的钒。在兔子身上有证据表明，钒可能通过减少缓激肽生成一氧化氮（内皮源性血管舒张因子）的合成和/或释放来发挥作用。本研究获得的功能、分析和形态学结果表明，长期接触钒引发动脉高血压的机制仅部分与接触水平、接触时间以及物种有关。
