Abstract
Salt-sensitive individuals show earlier and more serious cardiac damage than nonsalt-sensitive ones. Some studies have suggested that microRNA-133a could reduce cardiac hypertrophy and myocardial fibrosis. The current study aims to investigate the different functions of high-salt intake on salt-sensitive (SS) rats and Sprague-Dawley (SD) rats and the involvement of microRNA-133a in these roles. After high-salt intervention, the left ventricular mass (LVW) and left ventricular mass index (LVMI) of the salt-sensitive high salt (SHS) group were obviously higher than those of the salt-sensitive low salt (SLS) group. However, the difference between the Sprague-Dawley high salt (DHS) group and the Sprague-Dawley low salt (DLS) group was not significant. Compared with SLS group, collagen I and connective tissue growth factor (CTGF) in the heart of SHS group were significantly higher, whereas no statistical difference was observed between the DHS group and the DLS group. Compared with low-salt diet, microRNA-133a in the heart of both strains were significantly decreased, but that in the SHS group decreased more significantly. These results suggest that high salt intervention could down-regulate the expression of myocardial microRNA-133a, which may be one of the mechanisms involved in myocardial fibrosis in salt-sensitive hypertension.
Highlights
Hypertension is a primary risk factor for cardiovascular events, and salt-sensitivity is an intermediate genetic phenotype of essential hypertension
Other studies have confirmed that salt-sensitive hypertension entails more serious cardiac hypertrophy and fibrosis and that high salt could directly lead to cardiac fibrosis independently of blood pressure [14]
We found that the expression of microRNA-133a was down-regulated both in Dahl SS rats and in SD rats, so we speculate that high-salt was likely to down-regulated microRNA expression via its effect on Renin–Angiolensin–Aodosterone System (RAAS)
Summary
Hypertension is a primary risk factor for cardiovascular events, and salt-sensitivity is an intermediate genetic phenotype of essential hypertension. High salt intake can elevate blood pressure, and directly result in heart [1], brain [2] and kidney [3] damage independently of blood pressure. High salt intake promotes hyperplasia and hypertrophy of the myocardial cells and facilitates collagen deposition in myocardial cells, resulting in myocardial fibrosis and cardiac hypertrophy [4]. Studies have shown that microRNA-133a is mainly expressed in cardiac and skeletal muscles. It has several physiological and pathological effects, such as cardiac development [6], atthythmia [7], apoptosia [8], and smooth muscle differentiation [9]. Reports have indicated that microRNAs may be broadly involved in the pathological process of hypertensive cardiac hypertrophy and myocardial fibrosis
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