Abstract
The close relationship between hypertension and dietary sodium intake is widely recognized and supported by several studies. A reduction in dietary sodium not only decreases the blood pressure and the incidence of hypertension, but is also associated with a reduction in morbidity and mortality from cardiovascular diseases. Prolonged modest reduction in salt intake induces a relevant fall in blood pressure in both hypertensive and normotensive individuals, irrespective of sex and ethnic group, with larger falls in systolic blood pressure for larger reductions in dietary salt. The high sodium intake and the increase in blood pressure levels are related to water retention, increase in systemic peripheral resistance, alterations in the endothelial function, changes in the structure and function of large elastic arteries, modification in sympathetic activity, and in the autonomic neuronal modulation of the cardiovascular system. In this review, we have focused on the effects of sodium intake on vascular hemodynamics and their implication in the pathogenesis of hypertension.
Highlights
The close relationship between hypertension and dietary sodium intake is widely recognized and supported by several studies
A large meta-analysis [9] showed that modest reduction in salt intake for four or more weeks causes a significant fall in blood pressure (BP) in both hypertensive and normotensive individuals, irrespective of sex and ethnic group, and larger reductions in salt intake are linked to larger falls in systolic BP [9]
The current health policies have not reached an effective achievement for the reduction of dietary sodium in the population and the positive effects of a reduced sodium intake on BP levels tend to decrease with time, owing to poor dietary compliance
Summary
Available evidence suggests a direct relationship between sodium intake and blood pressure (BP). The mechanism of pressure natriuresis has been proposed as a physiologic phenomenon where an increase in BP in the renal arteries causes increased salt and water excretion [10]. This hemodynamic load, as studies with animal models have shown [11,12], may lead to an adverse microvascular remodeling by the effects of increased BP levels. We have first addressed the debate on salt-sensitivity, in light of recent evidence, and discussed the effects of sodium handling on arterial function and structure
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