Sodium restriction modulates innate immunity and prevents cardiac remodeling in a rat model of metabolic syndrome

Abstract

In the view of the relationships between excessive sodium intake, immunity and target organ damage, we hypothesized that reduction in dietary sodium would be beneficial in the prevention of cardiac alterations through a restrained local immunity response in a rat model of metabolic syndrome. Sprague-Dawley rats were fed a 60% fructose diet with either a normal sodium (0.64% NaCl) or a low sodium content (<0.01% NaCl) for 8weeks. After 4weeks, rats were infused or not with angiotensin II (200ng·kg·min, sc) for 4weeks. Tail-cuff blood pressure was determined in conscious rats. Heart and left ventricle weight, cardiomyocyte size, and cardiac fibrosis were evaluated. We performed a transcriptomic analysis in order to identify differentially regulated cardiac mRNAs between normal and low sodium diets. We validated those results using qPCR and immunohistochemistry. Angiotensin II-induced blood pressure rise was blunted (~50%) in the low-sodium fed rats while cardiac hypertrophy and fibrosis were prevented. Transcriptomic analysis revealed 66 differentially regulated genes including 13 downregulated genes under the low sodium diet and implicated in the innate immune response. This was confirmed by reduced cardiac macrophages infiltration under the low sodium diet. Dietary sodium restriction prevents structural alterations of the heart of rats with fructose-induced insulin resistance and angiotensin II-hypertension. The reduction of cardiac inflammation and macrophage infiltration suggests that innate immunity has an important role in the beneficial effect of sodium restriction on cardiac remodeling.

New Noonan syndrome model mice with RIT1 mutation exhibit cardiac hypertrophy and susceptibility to β-adrenergic stimulation-induced cardiac fibrosis

“…15). Consistent with other reports [48,49], the percentages of fibrosis area in the hearts from saline-treated Rit1 +/+ and Rit1 A57G/+ mice were higher (0.41 ± 0.10 and 0.59 ± 0.10, respectively) (Fig. 4c), than those in non-treated Rit1 +/+ and Rit1 A57G/+ mice (0.17 ± 0.04 and 0.38 ± 0.04) (Fig.…”

The effect of venlafaxine on blood pressure and ECG in rats fed with high-fat-fructose diet

“…Lower heart weight/body weight index was observed in group HFFD 5+3, and the administration of venlafaxine caused a decrease in heart weight independently from the length of HFFD. Other studies showed that in animal models of metabolic syndrome, with a high fructose diet, abnormalities in myocardial structure (Cheng et al, 2014) and cardiac hypertrophy were present (Delbosc et al, 2005;Jover et al, 2017). Due to a high intake of fat and fructose, hepatic and intracardial lipid accumulation was previously observed, which could affect not only morphology but also the function of the organs.…”