Centrally mediated effect of vanadate on diuresis and natriuresis in normal rats. Interaction with ouabain.

Prolonged infusion of vanadate (VO-3) (51 ng/microliter/hr during 15 hr), an in vitro inhibitor of Na,K-ATPase activity, into the 3rd brain ventricle (3BV) increased diuresis, sodium and potassium excretion in normal rats (p less than 0.001). Since the animals did not receive food or water during the infusion period, the effect of VO-3 was not related to hydration or volume expansion. A single injection of ouabain (a specific inhibitor of the sodium pump) 1 microliter, 50 pg/microliter, followed by a single injection of vanadate (1 microliter/51 ng/microliter) 1, 5 or 10 minutes after ouabain, prevented the diuretic and natriuretic effect of VO-3. When vanadate injections were delayed 20 or 30 minutes, diuresis reappeared. Ouabain (50 pg) decreased sodium intake induced by sodium depletion, an effect that lasted for 10 to 15 minutes after injection, a time coincident with the inhibition of the natriuretic effect of VO-3 by OUA. Then the life-span of ouabain effect on prevention of VO-3-induced diuresis as well as on inhibition of sodium intake, lasted between 10 to 15 minutes. These results provide further evidence for the powerful diuretic, natriuretic and kaliuretic effect of centrally injected vanadate. However, the finding that ouabain suppresses this effect, does not support the suggestion that the active transport system might be involved.