The importance of dietary salt in the development of hypertension has long been a source of controversy. Recent studies suggest a combination of high salt and angiotensin II infusion may increase sympathetic drive however the effect of a change in dietary salt alone is unclear. Using telemetry we recorded renal sympathetic nerve activity (RSNA), arterial pressure (MAP) and heart rate (HR) in 7 New Zealand white rabbits before and during a six day period of increased salt intake (normal NaCl 0.5g/kg/day, high NaCl 2.5g/kg/day) and a second group of 7 rabbits with normal salt intake throughout. The responses to stressful stimuli encountered in the laboratory were recorded and compared to rest in control and high salt groups. Resting MAP, HR and RSNA were not significantly altered with high salt intake (88±5 vs. 91±6 mmHg; 251±8 vs. 244±9 bpm; 9.7±1.2 vs. 10.8±1.7 n.u.) despite significant reductions in plasma renin activity (1.88±0.18 vs. 1.27±0.15 nmol Ang I.L-1.hour; p<0.05) and angiotensin II (7.5±1.2 vs. 4.3±0.8 pmol.L-1). Increasing levels of stressful stimuli (resting in home cage, containment in box, handling and nasopharyngeal activation) in animals on a normal salt diet caused graded increases in MAP (89±2 mmHg; 95±2 mmHg; 107±4 mmHg; 122±5 mmHg respectively) and RSNA (9.7±0.9 nu; 11.8±2.7 nu; 31.4±3.7 nu; 100 nu) but not HR (245±8 bpm; 234±8 bpm; 262±9 bpm; 36±5 bpm). High dietary salt did not significantly alter the responses to stress. We conclude that a six-day period of high salt intake does not alter the level of RSNA, with non-neural mechanisms primarily responsible for the observed renin-angiotensin system suppression.