Tj. Moore et al., SALT SENSITIVITY OF HYPERTENSION AND RESPONSES TO ANGIOTENSIN-CONVERTING ENZYME-INHIBITION WITH BENAZEPRIL, American journal of hypertension, 9(1), 1996, pp. 54-60
Salt intake, and the sensitivity of blood pressure (BP) to excessive s
alt intake is thought to contribute to the pathogenesis of essential h
ypertension in some patients. This study was designed to ascertain whe
ther salt sensitivity of BP is a determinant of BP and renal vascular
responsiveness to angiotensin converting enzyme (ACE) inhibition. In 2
4 patients with essential hypertension, ranging in age from 30 to 68 y
ears, renin status,renal hemodynamics, and sensitivity of BP to steady
state changes in salt intake were assessed. Twenty-four hour ambulato
ry BP monitoring (ABPM) was employed to measure baseline BP and BP res
ponse to 4 weeks' treatment with benazepril at 20 or 40 mg/day. Benaze
pril induced a highly-significant reduction in BP (P <.001) and increa
se in renal plasma flow (530 +/- 17 to 580 +/- 19 mL/min/1.73 m(2): 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). Th
e magnitude of the BP and renal vascular response to ACE inhibition wa
s not influenced by the sensitivity of BP to salt intake. In a multiva
riate analysis neither body mass index nor age influenced the BP respo
nse to ACE inhibition or the relationships between salt intake and a B
P response to ACE inhibition. We conclude that the factors that influe
nce sensitivity of BP to salt intake do not influence the systemic or
renal hemodynamic response to ACE inhibition.