VANADATE AS FACTOR OF CARDIOVASCULAR REGULATION BY INTERACTIONS WITH THE CATECHOLAMINE AND NITRIC-OXIDE SYSTEMS

The effects of 1 mu g/mL of vanadium, given for 12 mo as sodium metava nadate in drinking water, on cardiovascular and biochemical indices of male rabbits were investigated. At the end of the exposure period, va nadium was more accumulated in bones and kidneys than in spleen and li ver; the cardiac ventricles and the aorta contained similar amounts of this element. Blood pressure and heart rate were unchanged in the van adate-exposed animals since the observed decrease of both cardiac inot ropism and stroke volume was counteracted by an increase of peripheral vascular resistance, with reduction of arterial blood flow. The arter ial levels of sodium, potassium and aldosterone were unmodified by van adate which, however, strongly raised those of noradrenaline, adrenali ne, L-DOPA, and dopamine. Vanadate caused a marked increase of the act ivity of monoamine oxidase in renal tubules and liver (probably in rel ation to the increased plasma catecholamine levels) and a reduction of that of glucose-6-phosphate dehydrogenase in the kidney. There was al so evidence that vanadium reduces synthesis and/or release of nitric o xide, the endothelium-derived vasodilating factor, likely through a re duced formation from bradykinin. It was concluded that vanadium may re present an environmental factor of altered cardiovascular homeostasis.