Effects of chronic administration of vanadate on blood pressure, heart rate and Na+/K+-ATPase activity in adult male wistar rats.

Cardiovascular effects of chronic vanadate consumption were investigated in this study. Male wistar rats were divided into five groups and each group was allowed to drink one of the following fluids: I) water; II) water containing 0.02 mg/ml sodium orthovanadate (Na3VO4, vanadate), III) 1% saline, IV) 1% saline containing 0.02 mg/ml vanadate, and V) water containing 0.2 mg/ml vanadate, for a period of six weeks. Changes in arterial pressure and heart rate were essentially similar in all the groups during the treatment period. At the end of six weeks, studies conducted under urethane anesthesia showed that pressor responses to norepinephrine (NE) were potentiated in saline, saline + low vanadate, and water + high vanadate groups when compared to that of water + low vanadate or water drinking groups. In all these three groups in which NE responses were altered, renal Na+/K+-ATPase activity was found to be significantly suppressed (25 to 35%). In contrast, pressor responses to angiotensin II (A-II) were significantly enhanced in all the groups receiving vanadate or saline when compared to that of the water group, and these changes occurred whether or not there was any change in renal Na+/K+-ATPase activity. The data suggest that the changes noted in cardiovascular responses to vasoconstrictor agents, are conducive to the development of high blood pressure; however, failure to note sustained increase in arterial pressure during the treatment period may be due to the fact that in these rats renal compensation was not compromised.