To examine if chronic sodium loading on the brain produces sustained increases in blood pressure, water intake, and sodium excretion, hypertonic (0.5 M and 1.5 M) and isotonic (0.15 M) NaCI solutions were infused into the third ventricle of Sprague-Dawley rats at a rate of 5.5 Itl/hr for 7 days. Intracerebroventricular infusion of 1.5 M NaCI significantly increased systolic blood pressure during the entire infusion period (+23±5 mm Hg on day 1 and +15±2 mm Hg on day 7, n=10, mean±SEM). Blood pressure rose insignificantly in the 0.5 M NaCI group, whereas it remained at the baseline levels in the 0.15 M NaCI group. The increases in water intake (day 2), positive water balance (day 2), and negative sodium balance (day 3) were observed in the 1.5 M NaCI group. On day 7, the 1.5 M NaCI group showed hyponatremia and low plasma osmolality and had higher plasma norepinephrine but not vasopressin compared with the 0.15 M NaCI group. In another series of study, depressor response to intravenous hexamethonium (20 mg/kg) in the 1.5 M NaCI group was greater than that in the 0.15 M NaCI group on both day 1 and 7. The depressor response to (CH2) 5 These events are accompanied by various neurohormonal changes such as stimulation of the sympathetic nervous system with suppression of the renal nerve activity, release of vasopressin, sodium pump inhibitor and atrial natriuretic factor, stimulation of the pituitary-adrenocortical axis, and suppression of the peripheral reninangiotensin system. 1 ' 35 -8 Both the sympathetic nervous system and vasopressin appear to mediate the pressor response to intracerebroventricularly administered hypertonic NaCI.3
59The central action of sodium might play an important role in the relation between salt and hypertension. The sympathetic nervous system and vasopressin may participate in several models