Background: Contemporary diets are typically high in salt and fructose and such a refined diet has been proposed to contribute significantly to the overall burden of non-communicable disease in the population. Exposure to salt diet throughout fetal and neonatal development via maternal diet induces hypertension in the adult offspring. No study has explored potential interactions between maternal intake of salt and/or fructose and characterised offspring cardiovascular response through the circadian cycle. Methods: Pregnant rats were fed purified food (±4% salt) with freely available water (±10% fructose) before (4 weeks), during (21 days) and after gestation to weaning (21 days). Offspring (n=5/6 males/females from n=5/6 dams per treatment; 4 treatment groups) were weaned onto standard chow diet and from 10 weeks of age acute and chronic cardiovascular responses to anxiety (becoming singly-housed i.e. removal of paired rat from cage), salt-loading (5 days 4% salt in the diet), fructose loading (5 days 10% fructose in drinking water) nitric oxide blockade (with L-NAME) and voluntary physical activity were assessed by in-dwelling telemeters (DSI International). Results: Prenatal exposure to high salt diet elicited hypertension (142/103 vs. 128/88 ± 3 mm Hg; P=0.003) and an exacerbated baroreflex during an acute episode of anxiety in male, but not female offspring. These effects were unrelated to tonic nitric oxide activity, since chronic blockade with L-NAME elicited similar physiological responses between groups. Prenatal exposure to high fructose diet elicited increased resting heart rate (by 15-20 ±8 beats min-1) and greater pressor responses to fructose intake in both male and female offspring, despite one magnitude greater voluntary physical activity in female vs. male offspring (≈957 vs. 81 m day-1). Furthermore, fructose-exposed offspring displayed a blunted circadian variation (i.e. non-dipping) cardiovascular pattern. Conclusions: This study has revealed long-term circadian cardiovascular effects of increased maternal salt or fructose intake in the adult offspring, despite little direct exposure themselves. The delayed cardiovascular effects are distinctly sex-specific and thus any anticipated cardiovascular deterioration with age for example with prolonged, rather than short-term, exposure to such refined nutrients is likely to manifest differently in males vs. females.