Effects of Lisinopril on Stress-Induced Peak Blood Pressure and Sodium Excretion: A Double-Blind Controlled Study

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A stress test was performed before (SI) 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 μmol/min. Stress-induced sympathetic stimulation was assessed by a significant in- crease in urinary norepinephrine (NE) excretion from 21 ± 10 to 26 ± 10μ,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 μ-mol/min), whereas this retention was significantly reduced by lisinopril (13 ± 27 vs 69 ± 60μ,mol/min).

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