Abstract
Epidemiologic data revealed that a low sodium intake might have a favorable influence on blood pressure throughout an individual's lifetime. Sodium restriction was reported to lead to a modest fall in blood pressure in some studies, although a few groups of hypertensive patients experienced a rise in blood pressure. Left ventricular hypertrophy has been demonstrated to be related to cardiovascular morbidity and mortality independent of other risk factors. Dietary salt intake participates in the hypertrophic process independent of other determinants. Thus, 24-hour urinary sodium excretion has been reported to correlate with left ventricular mass independent of levels of arterial pressure. Three different mechanisms may link dietary salt intake to myocardial hypertrophy: the renin-angiotensin-aldosterone system, the sympathetic nervous system, and fluid volume homeostasis. Whether salt restriction reduces cardiovascular structural damage independent of arterial pressure has not been determined.
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