.-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-h AP, sodium, and water balances were measured in RDNX (n ϭ 11) and sham (n ϭ 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 after the 5-day period of normal salt (0.04% NaCl) intake (RDNX; n ϭ 6, sham; n ϭ 5). In protocol 1, AP was lower in RDNX (91 Ϯ 1 mmHg) compared with sham (101 Ϯ 2 mmHg) rats during the 5-day 0.4% NaCl control period. During the 10 days of high salt intake, AP increased Ͻ5 mmHg in both groups so that the difference between sham and RDNX rats remained constant. In protocol 2, AP was also lower in RDNX (93 Ϯ 2 mmHg) compared with sham (105 Ϯ 4 mmHg) rats during the 5-day 0.4% NaCl control period, and AP did not change in response to 10 days of a 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. sympathetic nervous system; angiotensin II; renal vascular resistance THE KIDNEYS PLAY A PROMINENT role in fluid and electrolyte regulation and therefore arterial pressure homeostasis. One mechanism by which the kidneys are thought to maintain fluid homeostasis is by the renal sympathetic nerves. Fluctuations in the degree of renal sympathetic nerve activity (RSNA) modulate renin secretion from juxtaglomerular cells, sodium reabsorption from renal tubular cells, and renal hemodynamics (13).Many lines of evidence have implicated sympathetically mediated mechanisms in the development of hypertension in several rat models (23,26,27,46). Accordingly, in some models of hypertension, complete renal denervation delayed the development of hypertension (23, 27-30). These results indirectly support a role of afferent and efferent renal nerves in the pathogenesis of hypertension. However, evidence suggesting that renal nerves are important in the long-term control of blood pressure in normotensive rats is not well established. For example, under conditions of increases in dietary sodium intake, is the reduction of RSNA important in the maintenance of a normotensive state? Although this is a crucial question, it has not been answered due to technical limitations for long-term recording of sympathetic nerve activity in conscious rats.The results of several studies (6, 33) tend to suggest that RSNA is modulated by changes in baroreceptor afferent nerve activity. The role of the baroreflex in regulating RSNA is in part sup...