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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) NaCl solutions were infused into the third ventricle of Sprague-Dawley rats at a rate of 5.5 microliters/hr for 7 days. Intracerebroventricular infusion of 1.5 M NaCl 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 NaCl group, whereas it remained at the baseline levels in the 0.15 M NaCl 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 NaCl group. On day 7, the 1.5 M NaCl group showed hyponatremia and low plasma osmolality and had higher plasma norepinephrine but not vasopressin compared with the 0.15 M NaCl group. In another series of study, depressor response to intravenous hexamethonium (20 mg/kg) in the 1.5 M NaCl group was greater than that in the 0.15 M NaCl group on both day 1 and 7. The depressor response to d(CH2)5Tyr(Me)-arginine vasopressin (10 micrograms/kg) in the 1.5 M NaCl group was greater on day 1 but not on day 7. These results indicate that sustained sodium stimulus on the central nervous system causes mild hypertension and alters water and sodium balance. The sympathetic nervous system but not vasopressin may play an important role in the chronic phase of central NaCl-induced hypertension.

Effects of chronic intraventricular sodium on blood pressure and fluid balance.