**1. Introduction**

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]. Hypertension guidelines frequently recommend salt reduction as an important simple strategy to reduce high blood pressure (BP) [2–4]. This recommendation is usually extended to individuals with normal BP as well as those at risk of becoming hypertensive [5].

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. The kidney excretes the excess of sodium, leading to normal blood pressure restoration. This hypothesis elucidates how blood pressure is sustained over the time, although the daily variation in sodium intake is reported among most individuals [6–8].

Excess dietary sodium consumption has several known detrimental effects on blood pressure [8–10] and has been associated with a higher risk of stroke and renal impairment [11, 12]. Accordingly, there is a strong evidence from randomized controlled trials that a moderate reduction in dietary salt intake safely and effectively reduces BP and urinary albumin excretion rate both in hypertensive and diabetic patients [13, 14]. Likewise, evidence from epidemiological and clinical studies also 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 also 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]. These changes on arterial wall are believed to be induced by both reduced bioavailability of nitric oxide and a deficient response of the local renin-angiotensin system to high sodium consumption [21]. Some interventional studies in man have investigated the effect of reduction in salt intake on arterial stiffness, but their results were not conclusive mainly because of the low statistical power of most of them [22–25].

Results from a systematic review and meta-analysis of the available clinical trials testing the effect of sodium intake restriction on PWV as a proxy for arterial stiffness, with null hypothesis being that restriction of sodium intake does not affect arterial stiffness, indicated that restriction of dietary sodium intake reduces arterial stiffness. The authors have suggested that this effect seems to be at least in part independent of the changes in blood pressure [26].

To date, the evidence on the effects of dietary sodium restriction on pulse wave velocity is still conflicting. Accordingly, this review aims to contribute to increase the knowledge about the effects of sodium restriction on arterial stiffness in the context of hypertension.

### **2. Effects of sodium reduction on blood pressure**

High sodium intake is linked to a higher risk of stroke, left ventricular hypertrophy, and renal impairment and can impair the arterial vasculature and endothelial function [10, 22, 27–29]. A moderate reduction in dietary sodium to achieve a sodium intake between 1.5 and 2.3 g/day may be cardioprotective independent of the BP pathway, but the evidence is not conclusive in this regard. It also may not be safe to recommend sodium restriction in older adults with diabetes or those with established CVD [3].

Evidence indicates that reducing sodium intake significantly lowers blood pressure in both men and women. Sodium is found not only in table of salt but also in a variety of foods, including cream, eggs, milk, shellfish, meat, and many other processed foods. The World Health Organization (WHO) recommendations indicate a reduction in sodium intake to lower blood pressure and risk of stroke, cardiovascular disease, and coronary heart disease in adults [30].

The current recommendations in most countries around the world are to reduce salt intake from about 9–12 g/day to 5–6 g/day [31]. Much evidence supports that such a reduction in salt intake lowers blood pressure. The WHO recommends a reduction to <2 g/day sodium (5 g/day salt) in adult individuals [30, 31].

The effects of sodium reduction on blood pressure have been evaluated in many studies. In their study that evaluated the effect of sodium reduction on blood pressure, D'Elia et al.'s [26] pooled analyses showed a significant reduction of both systolic blood pressure (SBP) (mean difference, −5.82 mmHg;

*The Effect of Dietary Sodium Restriction on Vascular Stiffness in Hypertension DOI: http://dx.doi.org/10.5772/intechopen.93090*

95% IC, −8.42 to −3.43 mmHg) and diastolic blood pressure (DBP) (mean difference, −2.75 mmHg; 95% IC, −3.67 to −1.87 mmHg) upon the reduction of sodium intake.

Evidence also shows that a modest reduction in salt intake for a couple of weeks (4 or more weeks) causes important and significant lowering in blood pressure levels in both normal and hypertensive individuals, independent of sex and ethnicity [13]. Salt reduction is linked to a mild increase in noradrenaline, aldosterone, and plasma renin activity, and no significant change in lipid concentrations. These results may support a reduction in population salt consumption, which would lower population mean blood pressure and thereby reduce cardiovascular risk outcomes. In their meta-analysis, He et al. [13] have shown that a modest reduction in salt intake, as currently recommended, has a significant effect on blood pressure both in individuals with hypertension and in those with normal blood pressure. The fall in blood pressure is seen in white and black individuals irrespective of their gender. These findings provide additional support for reducing salt intake in the population.
