Abstract
Increased salt consumption is believed to induce high blood pressure (BP)-mediated organ damage, although it is not yet clear whether it reflects a generalized micro- and macrovascular malfunction independent of BP. Exceeding dietary sodium intake is acknowledged to be the main modifiable environmental risk factor for cardiovascular events that accounts for an increase in blood pressure and induces hypertension (HTN)-related target organ damage. Arterial stiffness is well known as an independent cardiovascular risk factor, and sodium intake may be a determinant of arterial stiffness. Even so, the studies that investigated the effect of dietary sodium reduction intake on arterial stiffness in humans provided inconclusive results. Therefore, we aim to perform a review of the available evidence of salt restriction and arterial stiffness and its impact on hypertensive patients.
Highlights
Hypertension (HTN) is a significant risk factor for cardiovascular disease (CVD), a major cause of premature death worldwide, and has been identified as one of the strongest risk factors in the global burden of disease [1, 2]
Evidence from studies of genetic models of animal hypertension suggested that long-term high sodium intake is associated with increased intima-media thickness due to the extracellular matrix (ECM) development and aortic hypertrophy regardless of blood pressure
Health recommendations and most clinical studies have been focused on the adverse effects of salt dietary on blood pressure
Summary
Hypertension (HTN) is a significant risk factor for cardiovascular disease (CVD), a major cause of premature death worldwide, and has been identified as one of the strongest risk factors in the global burden of disease [1, 2]. The pressure-natriuresis mechanism that was first described by Guyton et al [6] proposes a linkage between dietary sodium intake and renal sodium handling This hypothesis says that, in normal individual, the consumption of high amounts of sodium in the diet will cause a transient increase in BP that promotes a higher excretion of sodium by the kidney. Evidence from epidemiological and clinical studies suggested an association between regular dietary salt intake and pulse wave velocity (PWV) [15–17] This association between dietary salt consumption and pulse wave velocity is supported by experimental evidence in animal models of structural and functional changes caused by high salt regimens on the arterial wall above and beyond the effect of high BP [18–20]. This review aims to contribute to increase the knowledge about the effects of sodium restriction on arterial stiffness in the context of hypertension
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