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1 ynthesis was blocked by aliskiren but not by benazepril.
3 ogs received three different dosages of oral benazepril (0.125 mg/kg, 0.25 mg/kg, or 0.5 mg/kg) in a
4 ce response system in a 1:1 ratio to receive benazepril (20 mg) plus amlodipine (5 mg; n=5744) or ben
5 il (20 mg) plus amlodipine (5 mg; n=5744) or benazepril (20 mg) plus hydrochlorothiazide (12.5 mg; n=
6 = 0.43, p = 0.0011) should be preferred over Benazepril 5.0 (r(2) = 0.9291, p < 0.0001) or Olmesartan
7 ere treated with insulin, candesartan (ARB), benazepril (ACE inhibitor), or aliskiren (renin inhibito
10 There were 552 primary-outcome events in the benazepril-amlodipine group (9.6%) and 679 in the benaze
11 dose adjustment were 131.6/73.3 mm Hg in the benazepril-amlodipine group and 132.5/74.4 mm Hg in the
12 representing an absolute risk reduction with benazepril-amlodipine therapy of 2.2% and a relative ris
13 ine, but rates were significantly lower with benazepril and amlodipine in overweight patients (hazard
14 both benazepril and hydrochlorothiazide and benazepril and amlodipine, but rates were significantly
17 , primary event rates were similar with both benazepril and hydrochlorothiazide and benazepril and am
18 ment with single-pill combinations of either benazepril and hydrochlorothiazide or benazepril and aml
22 ascular endpoint (for amlodipine, amlodipine-benazepril, and quinapril), non-vertebral fracture (for
23 -converting enzyme inhibitors (ACEI) such as benazepril are commonly prescribed in both humans and do
25 fects of a renin-angiotensin system blocker, benazepril, combined with amlodipine (B+A) or hydrochlor
26 ociated with the response of diastolic BP to benazepril (diastolic BP response: -7.4 mm Hg for subjec
27 ere collected at serial time intervals after benazepril dosing to measure plasma benazeprilat (active
28 -name products for amlodipine and amlodipine-benazepril (HR [95% CI]: 0.91 [0.84-0.99] and 0.84 [0.76
29 l-amlodipine combination was superior to the benazepril-hydrochlorothiazide combination in reducing c
30 epril-amlodipine group (9.6%) and 679 in the benazepril-hydrochlorothiazide group (11.8%), representi
32 AAS); however, the dose-dependent effects of benazepril on comprehensive RAAS components remain unkno
33 rs [SD 0.4]) because of superior efficacy of benazepril plus amlodipine compared with benazepril plus
34 of chronic kidney disease progression in the benazepril plus amlodipine group compared with 215 (3.7%
35 sease, angio-oedema was more frequent in the benazepril plus amlodipine group than in the benazepril
37 ular events to receive treatment with either benazepril plus amlodipine or benazepril plus hydrochlor
39 d that initial antihypertensive therapy with benazepril plus amlodipine was superior to benazepril pl
40 hronic kidney disease was peripheral oedema (benazepril plus amlodipine, 189 of 561, 33.7%; benazepri
41 43 (1%) patients who were lost to follow-up (benazepril plus amlodipine, n=70; benazepril plus hydroc
42 dipine group compared with 215 (3.7%) in the benazepril plus hydrochlorothiazide group (HR 0.52, 0.41
43 a, and hypotension were more frequent in the benazepril plus hydrochlorothiazide group than in the be
45 h benazepril plus amlodipine was superior to benazepril plus hydrochlorothiazide in reducing cardiova
46 dipine should be considered in preference to benazepril plus hydrochlorothiazide since it slows progr
47 nazepril plus amlodipine, 189 of 561, 33.7%; benazepril plus hydrochlorothiazide, 85 of 532, 16.0%).
51 ted 1447 hypertensive patients from a 3-year benazepril postmarket surveillance trial and genotyped t
52 were partially inhibited by candesartan and benazepril, whereas aliskiren produced complete inhibiti