Role of cellular calcium in salt sensitivity of patients with essential hypertension.

Abstract

The mechanism by which excessive sodium chloride intake raises blood pressure has not been fully clarified. The present study was therefore undertaken in patients with essential hypertension to investigate the possible role of an intracellular calcium-dependent mechanism in salt sensitivity. The difference in mean blood pressure between a week of low sodium chloride diet (3 g/day) and a week of high sodium chloride diet (20 g/day) was studied in relation to the intracellular free calcium concentration in lymphocytes and an acute hypotensive response to a 10-mg sublingual dose of nifedipine in 12 inpatients. Sodium chloride loading induced significant increases in mean blood pressure (from 111 +/- 12 to 122 +/- 11 mm Hg; p less than 0.01), intracellular free calcium in lymphocytes (from 133 +/- 13 to 145 +/- 9 nmol/L; p less than 0.01), and the hypotensive response to nifedipine (from 19 +/- 6 to 31 +/- 10 mm Hg; p less than 0.01). In addition, serum total calcium concentration was decreased while urinary calcium excretion was increased. The elevation of mean blood pressure was closely and positively correlated with the increase in intracellular free calcium concentration (r = 0.71, p less than 0.05) and the increase in the hypotensive effect of nifedipine (r = 0.91, p less than 0.01) after sodium chloride loading. However, changes in these values had no relation to the change in serum concentration or urinary excretion of calcium. These data suggest that change in the cellular calcium-dependent vasoconstriction mechanism may be associated with salt sensitivity of patients with essential hypertension.