Background: The association between cardiovascular health and salt intake remains controversial.

Methods: In 630 participants (mean age 40.6 years; 51% women), randomly recruited from F. alemish population, we measured sodium and creatinine in 24 hour urine samples at baseline and follow-up (median, 9.7 years) and the carotid and aortic augmentation indexes (AI) standardized to heart rate at follow-up only.

Results: The carotid AI (130.2% vs 113.7%) and aortic AI (145.7 vs 127.4) were higher (P<0.0001) in women than men and increased with age (10.1% and 8.5% per 10 years). From baseline to follow-up, the urinary sodium concentration decreased (117.1 vs 105.2 mmol/L; P<0.0001), whereas 24 hour urinary sodium did not change (166.5 vs 171.5 mmol; P=0.12). In multivariable-adjusted longitudinal analyses, a 40 mmol/L (∼1 SD) increase in the urinary sodium concentration at baseline was independently and inversely associated with the carotid AI (effect size, 1.38±0.66%; P=0.038) and aortic AI (1.54±0.72%; P=0.019). In cross-sectional analyses of follow-up data, these estimates were 1.26±0.70% (P=0.07) and 1.52±0.76% (P=0.045), respectively. In the longitudinal and cross-sectional analyses, the carotid and aortic AIs were unrelated to the 24 hour urinary excretion of sodium (P≥0.43).

Conclusions: Our study showed an inverse association between the AIs in the central arteries and the urinary sodium concentration, but not sodium excretion. Vasodilatation of the afferent renal arterioles in response to higher sodium concentration is mediated via the connecting tubule glomerular feedback mechanism; this might move reflection sites in the renal arteries more distally and thereby explain our observations.