It has been known that vanadium is a trace element which is essential for normal development and growth of animals and that it inhibits Na-K-ATPase as well. Though the cellular activity of vanadate is similar to that of ouabain in some respect, it does not faithfully mimic all of the effects of cardiac glycosides.
Recently it was reported that intravenously administered vanadate can alter heart rate and arterial presure in anesthetized animals.
The present study was undertaken to investigate effects of vanadate on arterial pressure and heart rate in conscious animals.
The results obtained were as follows:
1. Following intravenous administration of 50pg/kg vanadate into unanesthetized, conscious cats heart rate decreased significantly, whereas arterial pressure remained unchanged. No difference was observed in cardiovascular responses to vanadate between anesthetized and unanesthetized groups.
2. When 200g/kg vanadate was infused into the vein of conscious animal, arterial pressure elevated slightly, while heart rate decreased markedly. Compared with anesthetized group, heart rate decreased significantly more, whereas no change was recognized in blood pressure response.
3. After intravenous administation of 400 g/kg vanadate into unanesthetized cats, heart rate slowed down significantly. On the other hand in anesthetized animals arterial blood pressure declined remarkably, while heart rate was reduced almost as much as in unanesthetized group.
4. During and following intravenous infusion of vanadate for 10 minutes (300 g/min) into conscious group blood pressure elevated by 13 minutes after starting of vanadate infusion. However no significant difference was recognized in cardiac rate and blood pressure response compared between unanesthetized and anesthetized group.
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