Salt sensitivity, a trait characterized by a pressor blood pressure (BP) response to increased dietary salt intake, has been associated with higher rates of cardiovascular target organ damage and cardiovascular disease events. Recent experimental studies have highlighted the potential role of the natriuretic peptides and aldosterone in mediating salt sensitivity.
Methods and Results:
We evaluated 1575 non-hypertensive Framingham Offspring cohort participants (mean age 55±9 years, 58% women) who underwent routine measurements of circulating aldosterone and N-terminal proatrial natriuretic peptide (NT-ANP) and assessment of dietary sodium intake. Participants were categorized as potentially ‘salt-sensitive’ if their serum aldosterone was >sex-specific median but plasma NT-ANP was ≤sex-specific median value. Dietary sodium intake was categorized as lower versus higher (dichotomized at the sex-specific median). We used multivariable linear regression to relate presence of salt sensitivity (as defined above) to longitudinal changes (Δ) in systolic and diastolic BP on follow-up (median 4 years). Participants who were ‘salt-sensitive’ (N=437) experienced significantly greater increases in BP (Δ systolic, +4.4 and +2.3 mmHg; Δ diastolic, +1.9 and −0.3 mmHg; on a higher versus lower sodium diet, respectively) as compared to the other participants (Δ systolic, +2.8 and +1.0 mmHg; Δ diastolic, +0.5 and −0.2 mmHg; on higher versus lower sodium diet, respectively; p=0.033 and p=0.0127 for differences between groups in Δ systolic and Δ diastolic BP, respectively).
Our observational data suggest that higher circulating aldosterone and lower NT-ANP concentrations may be markers of salt sensitivity in the community. Additional studies are warranted to confirm these observations.
Keywords: salt sensitivity, aldosterone, N-terminal proatrial natriuretic peptide, ANP