RENAL NEUROGENIC MEDIATION OF INTRACEREBROVENTRICULAR ANGIOTENSIN-II HYPERTENSION IN RATS RAISED ON HIGH SODIUM-CHLORIDE DIET

Chronic elevation of sodium intake may affect the sensitivity of the c entral nervous system to intracerebroventricular (ICV) angiotensin II (Ang II) infusion. Experiments were conducted to determine the influen ce of raising Sprague-Dawley rats from 2 to 3 weeks of age on low (5.0 mmol/L per kg food), normal (50 mmol/L per kg food), or high (250 mmo l/L per kg food) NaCl diets on renal and cardiovascular responses to l ow-dose ICV Ang II infusion. kt 12 weeks of age, Sprague-Dawley rats w ere instrumented for chronic study, including brain lateral ventricula r cannulation. Artificial cerebrospinal fluid was infused (0.25 mu L/m in ICV) during control and recovery, whereas Aug II (20 ng/min) was in fused for 5 days. During the experiment, respective sodium intakes wer e infused intravenously over 24 hours. In rats fed high sodium, contro l mean arterial pressure was 115+/-2 mm Hg and increased to 132+/-4 mm Hg by day 5 of ICV Ang II infusion. This increase in arterial pressur e was associated with significant (P<.05) decreases in sodium excretio n, leading to the retention of 5.4+/-0.6 mmol/L total sodium over the 5 daps of Ang II infusion. Ln rats raised on low and normal sodium int akes from weaning and in 10-week-old rats exposed to a high sodium die t for only 2 weeks, arterial pressure was not increased and sodium was not retained during ICV Ang II infusion at 20 ng/min. In rats raised on the high sodium diet, bilateral renal denervation abolished the art erial hypertension and reduced the sodium retention over 5 days of ICV Ang II infusion. Thus, chronic elevation of sodium intake increases t he hypertensive response to low-dose ICV Ang II infusion, which is dep endent on intact renal nerves. We conclude that elevated postnatal NaC l intake enhances the presser sensitivity of the brain to Ang II.