In order to assess the impact of dietary sodium intake on the degree of left ventricular hypertrophy, we determined posterior wall thickness, relative wall thickness and left ventricular mass by two-dimensionally guided M-mode echocardiography, and related these parameters to sodium excretion over 24 h. There was no restriction on sodium intake. The first cohort comprised 43 subjects (residents of New Orleans) with mild to moderate essential hypertension who had not been treated for at least 4 weeks; in this cohort sodium excretion correlated with posterior wall thickness (r = 0.64, P less than 0.001), relative wall thickness (r = 0.67, P less than 0.001) and left ventricular mass (r = 0.37, P less than 0.02). A stepwise multiple regression analysis confirmed that sodium excretion was a determinant of posterior wall thickness (P less than 0.02) and relative wall thickness (P less than 0.05) independently of age, arterial pressure and body weight. The second cohort comprised 60 white male patients (residents of Bonn) with mild essential hypertension who had never been treated in the past; in this cohort sodium excretion correlated with diastolic diameter (r = 0.36, P less than 0.001) and with left ventricular mass (r = 0.35, P less than 0.001). Sodium excretion and systolic pressure emerged as independent variables (P less than 0.02) for left ventricular mass as evaluated by multiple regression analysis. These results identify dietary sodium intake as an independent powerful determinant of left ventricular hypertrophy in two disparate patient cohorts. Thus, for a similar haemodynamic load, sodium intake might accelerate, and conversely salt restriction mitigate, cardiac structural adaptation in patients with essential hypertension.