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* To whom correspondence should be addressed. E-mail: osbor003{at}umn.edu.
The present study was designed to test the hypothesis that renal nerves chronically modulate arterial pressure (AP) under basal conditions, and during changes in dietary salt intake. To test this hypothesis, continuous telemetric recording of AP in intact (SHAM) and renal denervated (RDNX) Sprague Dawley rats was performed and the effect of increasing and decreasing dietary salt intake on AP was determined. In protocol 1, 24-hour AP, sodium, and water balances were measured in RDNX (n = 11) and SHAM (n = 9) rats during 5 days of normal (0.4% NaCl) and 10 days of high (4.0% NaCl) salt intake followed by a 3-day recovery period (0.4% NaCl). Protocol 2 was similar with the exception that salt intake was decreased to 0.04% NaCl for 10 days following the 5-day period of normal salt (0.04% NaCl) intake (RDNX; n = 6, SHAM; n = 5). In protocol 1, AP was lower in RDNX (91 ± 1 mm Hg) compared to SHAM (101 ± 2 mm Hg) rats during the 5-day 0.4% NaCl control period. During the 10 days of high salt intake, AP increased less than 5 mm Hg in both groups such that the difference between SHAM and RDNX rats remained the constant. In protocol 2, AP was also lower in RDNX (93 ±2 mm Hg) compared to SHAM (105 ±4 mm Hg) rats during the 5-day 0.4% NaCl control period and AP did not change in response to 10 days of low salt diet in either group. Overall, there were no between group differences in sodium or water balance in either protocol. We conclude that renal nerves support basal levels of AP irrespective of dietary sodium intake in normal rats.
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