Effect of intracerebroventricular vanadate administration on salt and water intake and excretion in the rat.

The effect of vanadate (VO-3), an "in vitro" inhibitor of Na,K-ATPase activity, on sodium and water intake and excretion of Na-depleted and water deprived rats, was investigated. Injection of sodium orthovanadate Na3V04, H20 14) 1 microliter, 1.0 mM solution, 51 ng/microliter free base vanadium (V) into the 3rd brain ventricle (3BV) inhibited by 34% the sodium intake induced by peritoneal dialysis (PD). Urinary water and sodium excretion increased and potassium excretion decreased. The same concentration of vanadate administered by continuous infusion into the 3BV (1 microliter/hr, 24 hr, 51 ng/microliter, 1.2 micrograms/24 hr) during 24 hours after PD, decreased sodium intake by 69%. The same rate of infusion through the jugular vein failed to inhibit sodium intake or to increase urinary water and sodium excretion. Injections into lateral hypothalamus were also ineffective. Vanadyl (VO+2), the reduced form of vanadate, did not affect sodium intake. Similar or larger doses of vanadate injected into the 3BV of water deprived rats, did not modify water intake significantly. The present results suggest that the Na-K, active transport system is involved in salt and water balance regulation at the central nervous system level.