Regulation of Sodium Excretion in Human Hypertension: Long-Term Effects of Calcium Antagonist and Angiotensin Converting Enzyme Inhibitor

Fourteen subjects with untreated essential hypertension were subjected to 2-h water immersion (WI) study. They were then randomly assigned to two distinct oral antihypertensive regimens with either calcium-channel blocker nifedipine (group l, n = 7) or the angiotensin-converting enzyme (ACE) inhibitor lisinopril (group 2, n = 7). Three months later, a WI study identical to the first was repeated in the same hypertensive subjects. In group 1, treatment with nifedipine gastrointestinal therapeutic system (30 mg daily) significantly enhanced the natriuretic response to volume expansion by WI (peak value 405 ± 82 μmol/min during WI plus nifedipine vs. 291 ± 52 μmol/min during WI alone, p < 0.05). In group 2, treatment with lisinopril (20 mg daily) was associated with a blunted natriuretic response to volume expansion by WI (peak value 189 ± 54 μmol/min during WI plus lisinopril vs. 320 ± 53 μmol/min during WI alone; p < 0.025). A significant direct correlation between urinary sodium excretion (δUNaV) and mean arterial pressure (δMAP) was noted during WI plus nifedipine. Each long-term drug treatment was associated with a decrease in BP and hormonal changes of the same magnitude. Our data suggest that calcium antagonists could act as “diuretic agents” capable of counteracting the antinatriuretic effect of reduced renal perfusion pressure.