Evidence for Centrally Mediated Effects of Vanadate on the Blood Pressure and Heart Rate in Anesthetized Dogs

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Abstract
Cerebroventricular administration of sodium orthovanadate (0.2 .mu.mol/kg per min for 20 min ivt [intraventricularly]) produced significant increases in the arterial blood of chloralose-anesthetized dogs. Following bilateral vagotomy, both arterial pressure and heart rate, were significantly elevated during ivt infusion. These effects were completely abolished when the animals were pretreated with an autonomic ganglionic blocker, hexamethonium. I.v. administration 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 i.v. vanadate were potentiated after hexamethonium, while the bradycardic effects were virtually eliminated. Vanadate apparently can produce cardiovascular alterations via neurogenic mechanisms. These centrally mediated effects and their relationship to Na pump inhibition should probably be given further consideration in evaluating the role in vanadium in the etiology of hypertension.

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