Summary

Excessive salt intake exacerbates hypertension and further increases left-ventricular mass
in clinical essential and experimental hypertension. Additionally, a growing body of
evidence strongly suggests that high dietary salt loading exerts detrimental cardiac effects
independently of its hemodynamic load. The clinical evidence of cardiac structural and
functional alterations associated with salt is, however, scarce. n order to explore the
purported beliefs in humans, in this review we draw on our experimental studies in
naturally occurring hypertension and discuss the clinical implications of the
nonhemodynamic mechanisms underlying these salt-related changes.
ntroduction
A large body of evidence has emerged from clinical epidemiological and interventional
investigations as well as experimental studies that have repeatedly identified a positive
relationship between salt and hypertension. The multinational ntersalt study clearly
related dietary sodium and blood pressure across many populations and, even more
difficult to demonstrate, within populations. n support of these epidemiological findings,
well-controlled clinical trials have provided strong evidence that reduction of sodium
intake lowers arterial pressure in both hypertensive and normotensive people.
n addition to elevated arterial pressure, left-ventricular hypertrophy !"#$% is an
independent cardiovascular risk factor in hypertension in association with impaired
coronary hemodynamics, ventricular fibrosis and dysfunction, and apoptosis. &ver many
years, clinical and experimental studies have demonstrated the additional potential of salt
to adversely affect cardiac structure and function independently of its influence on arterial
pressure. This finding is exceedingly important since only a small fraction of
hypertensive patients are said to demonstrate S&'()-SE*ST#E $+,E-TE*S&*.
n some large epidemiological studies, but not in others, high sodium intake has notably
been indicated as a strong and independent contributor to increased cardiovascular risks
and mortality.
This review summari.es the increasing strong clinical and experimental evidence that
supports the concept that sodium, rather than simply elevating arterial pressure, has a far
more complex role in hypertension. Although not comprehensive, we present compelling
evidence for a pattern of cardiac structural and functional changes that accounts for the
observed cardiovascular risk of increased sodium consumption. /here clinical evidence
is less strong, we add our experience from studies with experimental naturally occurring
hypertension to provide important clinical relevance and to establish the validity for
further clinical investigation.