Abstract
First described in 1955 by Jerome W. Conn, primary aldosteronism (PA) today is
well established as a relevant cause of secondary hypertension and accounts for
about 5–10 % of hypertensives. The importance of considering PA
is based on its deleterious target organ damage far beyond the effect of
elevated blood pressure and on PA being a potentially curable form of
hypertension. Aside the established contributory role of high dietary salt
intake to arterial hypertension and cardiovascular disease, high salt intake is
mandatory for aldosterone-mediated deleterious effects on target-organ damage in
patients with primary aldosteronism. Consequently, counselling patients on the
need to reduce salt intake represents a major component in the treatment of PA
to minimize cardiovascular damage. Unfortunately, in PA patients salt intake is
high and far beyond the target values of 5 g per day, recommended by the
World Health Organization. Insufficient patient motivation for lifestyle
interventions can be further complicated by enhancing effects of aldosterone on
salt appetite, via central and gustatory pathways. In this context, treatment
for PA by adrenalectomy results in a spontaneous decrease in dietary salt intake
and might therefore provide further reduction of cardiovascular risk in PA than
specific medical treatment alone. Furthermore, there is evidence from clinical
studies that even after sufficient treatment of PA dietary salt intake remains a
relevant prognostic factor for cardiovascular risk. This review will focus on
the synergistic benefits derived from both blockade of aldosterone-mediated
effects and reduction in dietary salt intake on cardiovascular risk.
Key words
salt intake - oxidative stress - aldosterone
