[Neurohumoral, autacoid and transductional mechanisms in the cardiovascular effects of vanadate: histochemical correlations]. / Meccanismi neuroumorali, autacoidali e trasduzionali negli effetti cardiovasali di vanadato: correlati istochimici.

ABSTRACT

Rabbits given 1 ppm of vanadate in drinking water for twelve months showed (a) increased plasma levels of catecholamines (b) reduction of the arterial concentration of nitric oxide (c) lower activity of urine kallikrein and higher activities of urine kininases I and II and enkephalinase (d) reduced cardiac inotropism and augmented total peripheral resistance, with unchanged blood pressure levels (e) accumulation of the metal in the aorta and cardiac ventricles. Monoaminooxidase and glucose-6-phosphate dehydrogenase activities were increased by vanadate in both kidney and liver and that of NADH-diaphorase in the kidney, in which NADPH-diaphorase activity was reduced. Some of the above results were also obtained in rats given 10 and 40 ppm of vanadate in drinking water for six-seven months; these animals showed arterial hypertension and reduced activity of Na, K-ATPase in the kidney. Vanadium appears to act on the cardiovascular function through selective neurohumoral, autacoidal and transductional mechanisms only in part depending on the species.