EFFECTS OF LISINOPRIL ON STRESS-INDUCED PEAK BLOOD-PRESSURE AND SODIUM-EXCRETION - A DOUBLE-BLIND CONTROLLED-STUDY

A stress test was performed before (S1) and after a 1-month treatment period (S2) in patients with essential hypertension, randomly allocated to receive either an angiotensin-converting enzyme inhibitor (ACEI), lisinopril (n=10), or placebo (n=10). The two groups were similar with regard to systolic and diastolic blood pressure (SBP, DBP), body weight, renal function, and 24-h sodium excretion. At Si, stress induced a significant increase in SBP of 18+/-9 mm Hg and in DBP of 10+/-6 mm Hg and a significant reduction in sodium excretion from 258+/-105 to 204+/-72 mu mol/min. Stress-induced sympathetic stimulation was assessed by a significant increase in urinary norepinephrine (NE) excretion from 21+/-10 to 26+/-10 mu g/g creatinine. One-month treatment by placebo did not change stress-induced BP reactivity, sodium retention, or urinary NE excretion. In the lisinopril group, rest and stress BP were significantly reduced by the treatment. Stress-induced sodium retention was higher after 1-month placebo treatment (72+/-78 vs 48+/-67 mu mol/min), whereas this retention was significantly reduced by lisinopril(13+/-27 vs 69+/-60 mu mol/min).