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1 so, whereas it was equivalent to those given lisinopril.
2 ice given anti-TGFbeta1 or the ACE inhibitor lisinopril.
3 -lisinopril, respectively, versus 1.9 nM for lisinopril.
4 ys of treatment with placebo, amlodipine, or lisinopril.
5 with and without pretreatment with unlabeled lisinopril.
6 e incidence of new-onset HFPEF compared with lisinopril.
7 : D(C4)lisinopril, D(C5)lisinopril, and D(C8)lisinopril.
8 tion: Treatment with sacubitril-valsartan or lisinopril.
9 in vitro with FBL, with and without 10(-6) M lisinopril.
10 those given chlorthalidone, amlodipine, and lisinopril.
11 assignment to chlorthalidone, amlodipine, or lisinopril.
12 s higher in the amlodipine (2.5-10 mg/d) and lisinopril (10-40 mg/d) arms compared with the chlorthal
13 ice were treated with Agt-ASO (66 mg/kg/wk), lisinopril (100 mg/kg/d), PBS (control), or scrambled AS
17 positron emission tomography in 17 patients (lisinopril: 9 patients, losartan: 8 patients) with hyper
20 ining the biodistribution of the 99mTc-[D(C8)lisinopril] analog in rats with and without pretreatment
21 roups to produce di(2-pyridylmethyl)amine(Cx)lisinopril analogs: D(C4)lisinopril, D(C5)lisinopril, an
22 t one level in 21 (13.2%) of 159 patients on lisinopril and 39 (23.4%) of 166 patients on placebo (od
23 dest BP changes and decreased adherence with lisinopril and absence of lipid differences with pravast
24 an ACE inhibitor (lisinopril) and placebo or lisinopril and an ARB (telmisartan), with the doses adju
26 een designed with potency similar to that of lisinopril and has been demonstrated to specifically loc
28 R) before and after long-term treatment with lisinopril and losartan in patients with hypertension an
29 The angiotensin converting enzyme inhibitor lisinopril and mineralocorticoid receptor (MR) antagonis
30 values ranging from 44 to 4500 nM for Ni-NTA-lisinopril and Ni-DOTA-lisinopril, respectively, versus
31 Early treatment with heart failure drugs lisinopril and spironolactone improves skeletal muscle p
33 three months of MR and decreased during both lisinopril and the combined therapy in which it was not
34 y-surface area) to receive an ACE inhibitor (lisinopril) and placebo or lisinopril and an ARB (telmis
35 (2) 75 mg aspirin, 40 mg simvastatin, 10 mg lisinopril, and 12.5 mg hydrochlorothiazide or to usual
36 (1) 75 mg aspirin, 40 mg simvastatin, 10 mg lisinopril, and 50 mg atenolol or (2) 75 mg aspirin, 40
37 hydroxy-beta-methylbutyrate, trichostatin A, lisinopril, and 6 from the glucocorticoid family) signif
41 opril (EDTA-lisinopril, NTA-lisinopril, DOTA-lisinopril, and GGH-lisinopril) conjugates were used to
43 ese results indicate that both diltiazem and lisinopril are safe for treatment of hypertension after
44 a and then randomly assigned them to receive lisinopril (at a dose of 10 to 40 mg per day) or placebo
46 GGH were linked to the lysine side chain of lisinopril by 1-ethyl-3-[3-(dimethylamino)propyl]carbodi
47 (M = technetium, rhenium) was conjugated to lisinopril by acylation of the epsilon-amine of the lysi
48 0.89-1.25), respectively, for amlodipine and lisinopril compared with chlorthalidone, and 10-year adj
50 dent inactivation of sACE-1 by metal chelate-lisinopril complexes revealed a remarkable range of cata
51 endent inhibition of sACE-1 by metal chelate-lisinopril complexes revealed IC(50) values ranging from
52 ting a more optimal orientation of M-chelate-lisinopril complexes within the active site of the N-dom
54 il, NTA-lisinopril, DOTA-lisinopril, and GGH-lisinopril) conjugates were used to form coordination co
55 where the distance of the chelator from the lisinopril core was investigated by varying the number o
57 bacute hemodynamic effects of amlodipine and lisinopril could contribute to the differences in CCA re
58 iron, cobalt, nickel, and copper, such that lisinopril could mediate localization of the reactive me
62 ked chelate-lisinopril (EDTA-lisinopril, NTA-lisinopril, DOTA-lisinopril, and GGH-lisinopril) conjuga
64 ted the effects found in rats medicated with lisinopril, except that cardiac ACE2 mRNA fell to values
68 the effectiveness and safety of diltiazem or lisinopril for treatment of hypertension after heart tra
69 o 35 mg daily, n=1568) of the ACE inhibitor, lisinopril, for 39 to 58 months, while background therap
71 t maximal coronary blood flow and MPR in the lisinopril group increased significantly compared with p
73 with chlorthalidone, randomization to either lisinopril (hazard ratio, 1.04; 95% confidence interval,
74 e had significantly lower risk than those on lisinopril (HR, 1.18 versus 2.57; P=0.04 for interaction
75 rophic mice treated with spironolactone plus lisinopril (IC50 0.1 nM) compared with untreated control
77 D(C5)lisinopril], IC50 = 144 nM; and Re[D(C4)lisinopril], IC50 = 1,146 nM, as compared with lisinopri
78 concentration of 50% (IC50) = 3 nM; Re[D(C5)lisinopril], IC50 = 144 nM; and Re[D(C4)lisinopril], IC5
79 inhibits angiotensinogen (Agt) synthesis to lisinopril in adult conditional Pkd1 systemic-knockout m
80 the effectiveness and safety of diltiazem or lisinopril in the treatment of hypertension in cyclospor
81 nce and absence of the antihypertensive drug lisinopril) in order to aid the understanding of how the
83 the length of the methylene spacer: Re[D(C8)lisinopril], inhibitory concentration of 50% (IC50) = 3
84 Compared with chlorthalidone, treatment with lisinopril is not associated with a meaningful reduction
86 after continuous administration of vehicle, lisinopril, losartan, or both drugs combined in their dr
89 ndomly assigned to receive labetolol (n=58), lisinopril (n=58), or placebo (n=63) between January, 20
90 an angiotensin-converting enzyme inhibitor (lisinopril; n = 8233), or an alpha-blocker (doxazosin; n
91 with one of the most widely used inhibitors, lisinopril (N2-[(S)-1-carboxy-3-phenylpropyl]-L-lysyl-L-
92 ulting amide-linked chelate-lisinopril (EDTA-lisinopril, NTA-lisinopril, DOTA-lisinopril, and GGH-lis
97 alidone, 5.6% with amlodipine, and 4.3% with lisinopril), or no diabetes at 2 years of in-trial follo
98 h the angiotensin converting enzyme blocker, lisinopril, or angiotensin II receptor blocker, losartan
100 ts randomized to chlorthalidone, amlodipine, lisinopril, or doxazosin treatments and followed up for
101 ) determined that treatment with amlodipine, lisinopril, or doxazosin was not superior to thiazide-li
102 re randomized to chlorthalidone, amlodipine, lisinopril, or doxazosin, providing an opportunity to co
103 the risk of HFPEF compared with amlodipine, lisinopril, or doxazosin; the hazard ratios were 0.69 (9
105 phagic, or intravenous labetalol, sublingual lisinopril, or placebo if they had dysphagia, within 36
106 ral randomisation to receive oral labetalol, lisinopril, or placebo if they were non-dysphagic, or in
108 omized and 34 [lisinopril/pravastatin (n=9), lisinopril/P-placebo (n=8), L-placebo/pravastatin (n=9),
109 emia with rosiglitazone or hypertension with lisinopril partially reduced ACR, consistent with indepe
112 an angiotensin-converting-enzyme inhibitor (lisinopril) plus an angiotensin-receptor blocker (telmis
113 y-seven participants were randomized and 34 [lisinopril/pravastatin (n=9), lisinopril/P-placebo (n=8)
114 sought to determine whether randomization to lisinopril reduces incident AF or atrial flutter (AFL) c
115 to 4500 nM for Ni-NTA-lisinopril and Ni-DOTA-lisinopril, respectively, versus 1.9 nM for lisinopril.
116 utralization of TGFbeta1 by anti-TGFbeta1 or lisinopril resulted in less collagen deposition and less
119 One het group received spironolactone and lisinopril starting at 8 weeks of life (het-treated-8);
120 as dramatically reduced by pretreatment with lisinopril, supporting ACE-mediated binding in vivo.
121 without significant differences between the lisinopril-telmisartan group and the lisinopril-placebo
122 composite primary outcome (hazard ratio with lisinopril-telmisartan, 1.08; 95% confidence interval, 0
125 so reduced in thyroids of anti-TGFbeta1- and lisinopril-treated mice compared with those of controls.
130 all of the CCA was significantly lower after lisinopril treatment than after amlodipine treatment (P
133 model showed relative risks of amlodipine or lisinopril versus chlorthalidone during year 1 were 2.22
134 idence intervals; P values) of amlodipine or lisinopril versus chlorthalidone were 1.35 (1.21 to 1.50
138 ity, whereas the combination of losartan and lisinopril was associated with elevated cardiac ACE2 act
139 hyperemic flow in the patients treated with lisinopril was not significantly different from correspo
141 nts as high as 150,000 M(-1) min(-1) (Cu-GGH-lisinopril), while catalyst-mediated cleavage of sACE-1
142 .77-1.42) than participants on amlodipine or lisinopril with incident diabetes (HR range, 1.22-1.53).
144 % of participants (chlorthalidone/amlodipine/lisinopril) with new-onset HFPEF versus 41.9% in those w
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