Effect of sodium intake on the hypotensive effect of calcium antagonists.

To clarify the influence of Na balance on the hypotensive effect of calcium antagonists, the changes of blood pressure and humoral factors after a single oral administration of 40 mg nicardipine were evaluated in 15 subjects with essential hypertension under high, normal, and low Na regimens (mean 24 hour urinary Na excretion: 320 +/- 24, 147 +/- 7, 27 +/- 6 mEq, respectively). Nicardipine induced a significant reduction of mean blood pressure and increase in heart rate. The change of mean blood pressure after nicardipine was negatively related to the pretreatment mean blood pressure under the three levels of Na intake (p less than 0.01). The slopes of the correlation lines for high, normal, and low Na regimens were -0.61, -0.69, and -0.52, respectively, without statistical significance. Nicardipine brought about significant increases in plasma renin activity and plasma norepinephrine, but no changes in plasma levels of epinephrine, 6-keto-prostaglandin F1 alpha, thromboxane B2 or serum aldosterone concentration. These results suggest that the magnitude of the untreated blood pressure and thereby the peripheral resistance are major determinants of the blood pressure fall caused by calcium antagonists, and that the failure to increase aldosterone and epinephrine in the face of peripheral vasodilation may be responsible in part for the hypotensive effect of this drug.