Aim
Phenotypic trajectories of aldosterone and renin during the transition to young adulthood, and their impact on vascular health have not been established. This study investigated whether changes in aldosterone and renin from adolescence to young adulthood correlate with markers of vascular function.
Methods
Participants from the community-based Raine Study with plasma aldosterone and direct renin measured at ages 17 and 27, and vascular assessments including aortic augmentation index (AIx) and aortic distensibility at age 27, were included. Multivariable linear regression models were employed to investigate associations between changes in aldosterone and renin from age 17 to 27 and vascular parameters at age 27. Causal mediation analysis was performed to evaluate whether blood pressure at age 27 mediated these associations.
Results
Among 610 participants (388 males, 222 females; 80% normotensive), aldosterone and renin significantly decreased from age 17 to 27 (mean aldosterone 416 to 287 pmol/L; renin 36.3 to 17.6 mU/L). In males, a smaller decrease in aldosterone, but not in renin, was independently associated with higher AIx (1.23 [95%CI 0.23−2.23]% per 100 pmol/L, p=0.016) and lower aortic distensibility (-0.27 [95%CI -0.50−-0.046] ×103 mmHg-1 per 100 pmol/L, p=0.019) at age 27, indicating worse arterial stiffness. The association with AIx was more pronounced in males with a greater-than-median renin reduction (<-10.6 mU/L) (2.61 [95%CI 0.97−4.26%] per 100 pmol/L, p=0.002). Mediation analysis indicated these relationships were largely attributable to direct effects, not mediated by blood pressure at age 27 (proportion mediated <6%). No associations were observed in females.
Conclusions
In young adult men, a blunted decline in aldosterone paired with a pronounced drop in renin may signal the emergence of renin-independent aldosterone production, associated with deteriorating vascular health largely independent of blood pressure. These findings suggest early renin-independent aldosterone production may drive cardiovascular risk before the onset of overt hypertension.