Salt sensitivity of hypertension and responses to angiotensin converting enzyme inhibition with benazepril

Salt intake, and the sensitivity of blood pressure (BP) to excessive salt intake is thought to contribute to the pathogenesis of essential hypertension in some patients. This study was designed to ascertain whether salt sensitivity of BP is a determinant of BP and renal vascular responsiveness to angiotensin converting enzyme (ACE) inhibition. In 24 patients with essential hypertension, ranging in age from 30 to 68 years, renin status, renal hemodynamics, and sensitivity of BP to steady state changes in salt intake were assessed. Twenty-four hour ambulatory BP monitoring (ABPM) was employed to measure baseline BP and BP response to 4 weeksʹ treatment with benazepril at 20 or 40 mg/day. Benazepril induced a highly-significant reduction in BP (P< .001) and increase in renal plasma flow (530 ± 17 to 580 ± 19 mL/min/1.73 m2; P< .001). Systolic BP fell from 143 ± 2 to 129 ± 2 mm Hg (P< .001), and diastolic BP fell from 91 ± 1.6 to 80 ± 2 mm Hg (P< .001). The magnitude of the BP and renal vascular response to ACE inhibition was not influenced by the sensitivity of BP to salt intake. In a multivariate analysis neither body mass index nor age influenced the BP response to ACE inhibition or the relationships between salt intake and a BP response to ACE inhibition. We conclude that the factors that influence sensitivity of BP to salt intake do not influence the systemic or renal hemodynamic response to ACE inhibition.