Experimental and clinical data suggest salt intake to be an important
factor in the pathogenesis of essential hypertension. However, the rel
ationship between dietary sodium and blood pressure has been found to
be relatively weak, perhaps because casual blood pressure levels fluct
uate considerably. We hypothesized that a closer correlation could be
expected between salt intake and the degree of hypertensive target org
an disease. We reviewed the literature for studies dealing with 24-hou
r urinary sodium excretion (as a measure of salt intake) and hypertens
ive target organ disease as assessed by left ventricular structure and
function, microproteinuria, cerebrovascular disease, and arterial com
pliance. Salt intake as assessed by 24-hour urinary sodium excretion w
as found to be a close independent determinant of left ventricular mas
s in 9 different studies worldwide. A reduction in dietary sodium has
been shown to reduce left ventricular hypertrophy. There is clinical a
nd experimental evidence, particularly in salt-sensitive patients, tha
t salt intake directly affects hypertensive renal disease, cerebrovasc
ular disease, and compliance of the large arteries. The close and part
ially independent correlation between salt intake and hypertensive tar
get organ disease suggests dietary sodium to be a direct perpetrator o
f cardiovascular disease.