Objective: Abnormal blood pressure (BP) rhythms precede and predict cardiovascular disease and are often linked with salt-sensitivity. The mechanisms underlying these rhythms are unknown. High dietary salt intake can cause phase shifts in the intrinsic circadian clocks within peripheral organs but the implications for BP rhythm are unclear. We investigated the effect of a high salt diet on the rhythms of BP, heart rate (HR) and activity. Design and method: BP was monitored by radiotelemetry in male C57BL6/J mice. After 1 week of 0.25% Na+ chow (baseline), mice received 3% Na+ diet for 3 weeks followed by 0.25% Na+ for a further 2 weeks (Na+ washout). Systolic BP (SBP), HR and activity data was analysed by cosinor analysis. Sympathetic nervous system activity was estimated by measuring 12 h urinary catecholamine spillover and plasma aldosterone was measured following a week of 3% Na+ diet. Results: Mesor (circadian mean) SBP increased by 7mmHg after week 1 of 3% Na+ diet. This was maintained over 3 weeks but reduced to baseline after Na+ washout. BP amplitude increased from 9mmHg (baseline) to 14mmHg within 1 week of 3% Na+ feeding. This was maintained for the 3 weeks of 3% Na+ but reduced to 8mmHg following Na+ washout. This reflected elevated active-phase BP rather than enhanced dip in sleep-phase BP. A ∼4.5-hour phase delay in SBP was observed in the second week of 3% Na+ diet. HR mesor did not change throughout the experiment but amplitude was elevated at 3 weeks of 3% Na+. Activity amplitude increased during the first week of 3% Na+ intake but was not maintained at week 2. Plasma aldosterone was appropriately suppressed but day and night urinary adrenaline levels were increased after 1 week on 3% Na+ diet. Conclusions: C57BL6/J mice exhibit salt-sensitive BP. A 3% Na+ diet altered BP rhythm by increasing amplitude and inducing a modest phase shift. Further studies are needed to investigate the role of the sympathetic system and intrinsic molecular clocks in the induction of these rhythms. This may give insights into mechanisms underlying the relationship between salt-sensitivity and abnormal BP rhythms.