ANG-II CHRONICALLY SUPPORTS RENAL AND LUMBAR SYMPATHETIC ACTIVITY IN SODIUM-DEPRIVED, CONSCIOUS RATS

The hypothesis that chronic elevations in endogenous angiotensin II (A NG II) increase sympathetic outflow in conscious, normotensive rats wa s tested by determining if acute blockade of ANG II receptors with los artan (10 mg/kg iv) decreases renal sympathetic nerve activity (RSNA), lumbar sympathetic nerve activity (LSNA), or heart rate (HR) more in rats with higher ANG II levels due to a low sodium (LS) diet compared with a control sodium (CS) or high sodium (HS) diet. In LS rats, losar tan decreased (P < 0.05) mean arterial pressure (MAP) in two phases: a n immediate decrease of 23 +/- 2 mmHg and a slower fall to 35 +/- 4 mm Hg below control 40 min postlosartan. Five minutes after losartan, RSN A (149 +/- 13%), LSNA (143 +/- 5%), and HR (109 +/- 2%) were increased (P < 0.05). Despite further falls in MAP the elevation in RSNA and HR remained constant, and LSNA decreased toward control (119 +/- 4%). Af ter restoration of MAP to basal levels with methoxamine or phenylephri ne infusion, RSNA (46 +/- 8%), LSNA (49 +/- 11%), and HR (76 +/- 2%) w ere suppressed (P < 0.05). In CS rats, losartan also initially decreas ed (P < 0.05) MAP by 6 +/- 2 mmHg and increased (P < 0.05) RSNA to 129 +/- 13%. When MAP was returned to control, RSNA was decreased (70 +/- 8%; P < 0.05) but less than in LS rats. In contrast, no changes in MA P, RSNA, LSNA, or KR were observed after losartan in HS rats. In concl usion, endogenous ANG II chronically supports RSNA, LSNA, and HR in co nscious, normotensive low and normal sodium intake rats.