The interface of aging and salt in driving salt-sensitive hypertension: a comparative study in aged and young rats

Hypertension prevalence is increasing in both aging and younger populations, with high salt intake being a key environmental driver. Whether young and aged individuals exhibit similar physiological and molecular responses to salt loading remains unclear. This study compared hemodynamic and renal redox adaptations to salt loading in young (8-week) and aged (50-week) Dahl salt-sensitive (DSS) rats. Both groups developed salt-sensitive hypertension, but blood pressure (BP) elevation was markedly lower in aged rats. High salt induced marked increases in stroke volume (SV), cardiac output (CO), and vascular indices, indicating strong cardiac and vascular contributions to BP rise. In contrast, aged rats displayed blunted increases in SV and CO, together with attenuated changes in vascular indices, reflecting diminished cardiac contractility and vascular responsiveness that accounted for their lower BP salt sensitivity. High salt disrupted redox homeostasis in both groups, but aged rats exhibited inherently reduced antioxidant capacity and greater renal oxidative stress, along with more pronounced glomerulosclerosis and interstitial fibrosis. Nitric oxide pathway suppression was more evident in young rats, whereas aged rats showed persistently low baseline NO availability. These findings demonstrate that aging reduces hemodynamic and vascular responsiveness to salt loading yet heightens susceptibility to salt-induced renal injury in DSS rats.