Epidemiologic data revealed that a low sodium intake might have a favo
rable influence on blood pressure throughout an individual's lifetime.
Sodium restriction was reported to lead to a modest fall in blood pre
ssure 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 morta
lity independent of other risk factors. Dietary salt intake participat
es 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. Thr
ee different mechanisms may link dietary salt intake to myocardial hyp
ertrophy: the renin-angiotensin-aldosterone system, the sympathetic ne
rvous system, and fluid volume homeostasis. Whether salt restriction r
educes cardiovascular structural damage independent of arterial pressu
re has not been determined.