Effect of Intracerebroventricular Administered Vanadate on Salt and Water Intake and Excretion in the Rat

Abstract

The activity of sensors mediating thirst and ADH release has been correlated to NaCl concentration of the brain CSF. Substances known to inhibit active trans-membrane enzymatic Na transport have been found to inhibit water intake and ADH release (1,2), suggesting that active Na transport may be essential for the excitation of cerebral sensors involved in water balance. Therefore, the discovery that vanadate, a natural occurring substance, is a potent “in vitro” inhibitor of Na, K-ATPase activity (3) made it an interesting “tool” to study water balance. In rats, acute sodium depletion by peritoneal dialysis produced dramatic changes in serum and CSF sodium concentration (4,5). Furthermore infusion of hypertonic artificial CSF into the 3rd ventricle decreased Na intake induced by sodium depletion (5). Therefore it was of interest to study whether an inhibitor of enzymatic Na-transport such as vanadate, would affect sodium and water intake and excretion in conscious rats.