Abstract
Abstract
Cerebroventricular administration of sodium orthovanadate (0.2 μ mole/kg/min for 20 min ivt) produced significant increases in the arterial blood pressure of chloraloseanesthetized dogs. Following bilateral vagotomy, both arterial pressure as well as heart rate were significantly elevated during ivt infusion. These effects were completely abolished when the animals were pretreated with an autonomic ganglionic blocker, hexamethonium. In contrast, intravenous administration (iv) of the same dose of vanadate significantly increased the arterial pressure only in the vagotomized dogs and this effect was accompanied by a reduction in the heart rate. Pressor effects of iv vanadate were potentiated after hexamethonium while the bradycardic effects were virtually eliminated. This study demonstrates that vanadate can produce cardiovascular alterations via neurogenic mechanisms. It is suggested that these centrally mediated effects and their relationship to sodium pump inhibition should be given further consideration in evaluating the role of vanadium in the etiology of hypertension.
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