Boscolo P, Carmignani M, Volpe A R, Felaco M, Del Rosso G, Porcelli G, Giuliano G
Centre of Occupational Safety and Ergophtalmology, University GD'Annunzio, Chieti, Italy.
Occup Environ Med. 1994 Jul;51(7):500-3. doi: 10.1136/oem.51.7.500.
The effects of 1, 10, or 40 micrograms/ml of vanadium, given for six or seven months as sodium metavanadate in drinking water on cardiovascular and biochemical variables and the electrolyte metabolism of male Sprague-Dawley rats were investigated. At the end of the exposure period, all animals exposed to vanadate had increased systolic and diastolic blood pressure. This effect was not dose dependent and heart rate and cardiac inotropism were not affected. The role of defective renal function and electrolyte metabolism in such effects was supported, in the rats exposed to 10 and 40 ppm of vanadium, by the following changes: (a) decreased Na, + K(+)-ATPase activity in the distal tubules of nephrons; (b) increased urinary excretion of potassium; (c) increase in plasma renin activity and urinary kallikrein, kininase I, and kininase II activities; (d) increased plasma aldosterone (only in the rats treated with 10 ppm of vanadium). The alterations in the rats exposed to 1 ppm of vanadium were: (a) reduced urinary calcium excretion; (b) reduced urinary kallikrein activity; (c) reduced plasma aldosterone. These results suggest that blood hypertension in rats exposed to vanadate depends on specific mechanisms of renal toxicity related to the levels of exposure.
研究了以偏钒酸钠形式，在饮用水中给予雄性斯普拉格-道利大鼠1、10或40微克/毫升钒，持续6或7个月，对心血管和生化变量以及电解质代谢的影响。在暴露期结束时，所有暴露于钒酸盐的动物收缩压和舒张压均升高。这种效应不依赖剂量，心率和心肌收缩力不受影响。在暴露于10和40 ppm钒的大鼠中，以下变化支持了肾功能缺陷和电解质代谢在此类效应中的作用：(a) 肾单位远端小管中Na, + K(+)-ATP酶活性降低；(b) 钾的尿排泄增加；(c) 血浆肾素活性以及尿激肽释放酶、激肽酶I和激肽酶II活性增加；(d) 血浆醛固酮增加（仅在给予10 ppm钒处理的大鼠中）。暴露于1 ppm钒的大鼠中的变化为：(a) 尿钙排泄减少；(b) 尿激肽释放酶活性降低；(c) 血浆醛固酮降低。这些结果表明，暴露于钒酸盐的大鼠中的高血压取决于与暴露水平相关的特定肾毒性机制。
