High salt intake deteriorates cardiac function of hypertrophied heart, possibly via excessive sympathetic drive

Abstract

Background: High salt intake often results in congestive heart failure in patients with left ventricular hypertrophy (LVH). We hypothesized that excessive sympathetic activation associated with salt intake plays a significant role in developing cardiac dysfunction.Methods and Results: We used ICR mice and applied aortic banding (AB) to create LVH. Four weeks after the banding, 24‐h urinary norepinephrine excretion (U‐NE) was higher in AB mice than in controls. LV function evaluated echocardiographically, however, was not different between groups. We then fed the mice a high salt diet (8%) for 4 weeks. LV function decreased in the AB mice compared with controls and was significantly worse in the high salt (HS)‐AB mice than in regular salt (RS)‐AB mice (LVDD: 3.5±1 vs 3.2±2 mm, wall thickness: 1.4±0.3 vs 1.2±0.1 mm, fractional shortening: 30±4 vs 44±1 %, all p<0.05). U‐NE was higher in HS‐AB than in RS‐AB mice. Further, the mice fed a high salt diet concurrent with AB developed LVH after 4 weeks, but LV systolic function remained normal without increases in U‐NE.Conclusions: In mice with LVH, high salt intake deteriorates cardiac function possibly through sympathetic overactivation. These results suggest that sympathetic activation plays a key role in the development of cardiac dysfunction.