ライフサイエンスコーパス: amlodipine

1 y targeted Ca2+ slow channels (diltiazem and amlodipine).

2 impairment (from the calcium channel blocker amlodipine).

3 symptoms despite maximum recommended dose of amlodipine.

4 P sensitivity to the calcium channel blocker amlodipine.

5 comparison of therapy based on valsartan or amlodipine.

6 and LTM dogs received placebo, atenolol, or amlodipine.

7 the response to bradykinin, enalaprilat and amlodipine.

8 lerotic effects of lovastatin, vitamin E and amlodipine.

9 th intracellular calcium mobility similar to amlodipine.

10 ent with amlodipine, and after withdrawal of amlodipine.

11 il and hydrochlorothiazide or benazepril and amlodipine.

12 316 to amlodipine, and 620 to aliskiren plus amlodipine.

13 ion therapy with 300 mg aliskiren plus 10 mg amlodipine.

14 plus placebo, or 150 mg aliskiren plus 5 mg amlodipine.

15 be treated successfully with octreotide and amlodipine.

16 uppressed by pretreatment with verapamil and amlodipine.

17 0 mg/kg given over first 6 hrs postburn); or amlodipine (0.07 mg/kg, 24 hrs preburn and 30 mins postb

18 gs each at quarter-dose (irbesartan 37.5 mg, amlodipine 1.25 mg, hydrochlorothiazide 6.25 mg, and ate

19 240 bpm, 3 weeks, n=8) or chronic pacing and amlodipine (1.5 mg . kg-1 . d-1, n=8).

20 enalaprilat: -0.7 +/- 0.5% to -26 +/- 1.2%; amlodipine: -1.3 +/- 0.9% to -18 +/- 1.2%; P < 0.05).

21 rug dose (6.5+/-6.1 and 3.4+/-3.9 ng/mL with amlodipine 10 and 5 mg, respectively, and -0.4+/-3.1 and

22 on 72-h electrocardiogram were randomized to amlodipine 10 mg once daily or diltiazem (Adizem XL) 300

23 8, hydrochlorothiazide 12.5 to 25 mg and/or amlodipine 10 mg was added if diastolic blood pressure w

24 mipril 10 mg/d (or irbesartan 300 mg/d), and amlodipine 10 mg/d were randomly assigned to renal dener

25 to treatment with irbesartan (300 mg daily), amlodipine (10 mg daily), or placebo.

26 sover study comparing the calcium antagonist amlodipine (10 mg once daily) versus isosorbide mononitr

27 nal classes III and IV randomized to receive amlodipine (10 mg/day) or placebo.

28 r week despite maximum recommended dosage of amlodipine (10 mg/day) were randomized to 1,000 mg ranol

29 ation of hydrochlorothiazide (25 mg/day) and amlodipine (10 mg/day).

30 Bradykinin (10(-4) mol/L, -21+/-5%), amlodipine (10(-5) mol/L, -14+/-5%), the ACE inhibitor r

31 Patients were randomized to receive amlodipine, 10 mg; enalapril, 20 mg; or placebo.

32 -13.9 +/- 1.9%, enalaprilat -15.3 +/- 1.6%, amlodipine -11.9 +/- 0.7%; WKY: bradykinin -22.8 +/- 1.0

33 sease was peripheral oedema (benazepril plus amlodipine, 189 of 561, 33.7%; benazepril plus hydrochlo

34 blocker BMS-186295 50 mg.kg-1.d-1 (n = 49), amlodipine 2.5 mg.kg-1.d-1 (n = 48) as a positive contro

35 pill were atorvastatin (at a dose of 10 mg), amlodipine (2.5 mg), losartan (25 mg), and hydrochloroth

36 w-onset heart failure (HF) was higher in the amlodipine (2.5-10 mg/d) and lisinopril (10-40 mg/d) arm

37 Responses to bradykinin (-2+/-6%), amlodipine (-2+/-4%), ramiprilat (-5+/-6%), and thiorpha

38 -22.8 +/- 1.0%, enalaprilat -24.1 +/- 2.0%, amlodipine -20.7 +/- 2.3%; P < 0.05), consistent with le

39 minutes after exercise in patients receiving amlodipine (3.5+/-1.4% versus 2.5+/-1.4%, P=0.014, and 5

40 s with chlorthalidone (-6.5 mm Hg) than with amlodipine (-3.8 mm Hg), lisinopril (-2.4 mm Hg), or dox

41 locker (acebutolol), (3) calcium antagonist (amlodipine), (4) diuretic (chlorthalidone), (5) alpha1-a

42 5%), enalaprilat (-37+/-5% vs. -23+/-5%) and amlodipine (-43+/-13% vs. -16+/-5%; p<0.05 from controls

43 , 62 patients were allocated to receive oral amlodipine 5 mg/day or placebo in addition to their curr

44 ded consisting of the sequential addition of amlodipine 5 mg/day, a standard dose of an angiotensin c

45 a dihydropyridine calcium channel blocker, (amlodipine 5-10 mg/d; n = 217).

46 1:1 ratio to receive benazepril (20 mg) plus amlodipine (5 mg; n=5744) or benazepril (20 mg) plus hyd

47 d fifty dentate patients who had been taking amlodipine, 5 mg per day for at least 6 months, voluntee

48 s from this group of patients indicated that amlodipine, 5 mg per day, did not induce gingival hyperp

49 rticipants were randomly assigned to receive amlodipine, 5 to 10 mg/d (n = 217), ramipril, 2.5 to 10

50 atment with either placebo (582 patients) or amlodipine (571 patients) for 6 to 33 months, while thei

51 Stunning occurred more often with ISMN than amlodipine (82% versus 48%).

52 ic relaxation period was less prolonged with amlodipine (93+/-15.5 versus 106.3+/-14.9 ms, P=0.018).

53 bined risk of fatal and nonfatal events with amlodipine (95 percent confidence interval, 24 percent r

54 percent reduction in the risk of death with amlodipine (95 percent confidence interval, 31 percent r

55 ns as cotreatment: a Mg2+-supplemented diet; amlodipine, a CCB; and N-acetylcysteine, an antioxidant.

56 1.1 in the presence of the bestselling drug amlodipine, a DHP antagonist (R)-(+)-Bay K8644, and a ti

57 92% (95% CI, 81.7 to 103.7) of baseline with amlodipine, a highly significant between-group effect (P

58 Amlodipine achieved a greater systolic and diastolic blo

59 There was no difference, however, between amlodipine (adjusted hazard ratio [HR], 0.46; 95% confid

60 significantly increased the availability of amlodipine (adjusted odds ratio [aOR] 2.84, 95% CI 1.10

61 Amlodipine also increased nitrite production in large co

62 Amlodipine also showed no effect on regression of hypert

63 red a composite cardiovascular endpoint (for amlodipine, amlodipine-benazepril, and quinapril), non-v

64 with generics versus brand-name products for amlodipine and amlodipine-benazepril (HR [95% CI]: 0.91

65 to examine a large group of patients taking amlodipine and determine the prevalence of gingival hype

66 in Europe (CAPE II) compared the efficacy of amlodipine and diltiazem (Adizem XL) and the combination

67 Both monotherapy with amlodipine and diltiazem (Adizem XL) were effective on s

68 t hospitalized HFPEF and HFREF compared with amlodipine and doxazosin.

69 ed by 4.8/2.5 mm Hg and 4.9/2.4 mm Hg in the amlodipine and enalapril groups, respectively (P<.001 fo

70 ose to null for the peripherally acting drug amlodipine and for other antihypertensive medications.

71 e second phase, atenolol 100 mg was added to amlodipine and isosorbide 5-mononitrate 100 mg to diltia

72 .12) and 1.05 (0.89-1.25), respectively, for amlodipine and lisinopril compared with chlorthalidone,

73 ences in the subacute hemodynamic effects of amlodipine and lisinopril could contribute to the differ

74 Amlodipine and lisinopril lowered BP similarly, but CCA

75 n the clinical composite outcome between the amlodipine and metoprolol groups.

76 we categorized patients into those receiving amlodipine and nonamlodipine CCBs.

77 The binding site for amlodipine and other dihydropyridines is located on the

78 The baseline amlodipine and placebo groups did not differ in demograp

79 disease, there was no difference between the amlodipine and placebo groups in the occurrence of eithe

80 s were undertaken in the treatment groups of amlodipine and placebo, and among those receiving backgr

81 lovastatin, the dihydropyridine Ca2+ blocker amlodipine and the antioxidant vitamin E.

82 In vivo, amlodipine and verapamil suppressed peritoneal macrophag

83 (2+) channel (LTCC) blockers, represented by amlodipine and verapamil, are widely used antihypertensi

84 /6.6 mm Hg for valsartan, 11.6/6.5 mm Hg for amlodipine) and at no time point was there a between-gro

85 re to less brain-penetrant dihydropyridines (amlodipine) and more brain-penetrant dihydropyridines (e

86 ertensive therapy (ramipril, metoprolol, and amlodipine) and two levels of BP control.

87 Of these, 442 were taking nifedipine, 181 amlodipine, and 186 diltiazem.

88 iabetes (7.5% with chlorthalidone, 5.6% with amlodipine, and 4.3% with lisinopril), or no diabetes at

89 lly allocated to aliskiren, 315 allocated to amlodipine, and 617 allocated to aliskiren plus amlodipi

90 were randomly assigned to aliskiren, 316 to amlodipine, and 620 to aliskiren plus amlodipine.

91 obtained at baseline, during treatment with amlodipine, and after withdrawal of amlodipine.

92 The effects of glyceryl trinitrate (GTN), amlodipine, and atenolol were studied in nine normal vol

93 140/80 mm Hg in those given chlorthalidone, amlodipine, and lisinopril.

94 n of assigned study medications (irbesartan, amlodipine, and placebo) on progressive renal failure an

95 g, angiotensin-converting enzyme inhibitors, amlodipine, and statins) can restore or maintain endogen

96 Amlodipine as well as approaches that cause store deplet

97 diltiazem (Adizem XL) and the combination of amlodipine/atenolol and diltiazem (Adizem XL)/isosorbide

98 ation therapy reduced ischemia further, with amlodipine/atenolol superior to diltiazem (Adizem XL)/is

99 Amlodipine/atenolol was significantly superior during th

100 Despite comparable levels of ischemia, amlodipine attenuated stunning when compared with ISMN.

101 in system blocker, benazepril, combined with amlodipine (B+A) or hydrochlorothiazide (B+H).

102 ear after randomization to atenolol-based or amlodipine-based antihypertensive treatment to assess LV

103 nd stroke events in individuals allocated an amlodipine-based combination drug regimen than in those

104 and 1.3 (SD 12.1) beats/min in atenolol- and amlodipine-based groups, respectively.

105 here was no evidence that the superiority of amlodipine-based over atenolol-based therapy for patient

106 Patients receiving treatment with an amlodipine-based regimen had better diastolic function t

107 d by both treatments, but the effects of the amlodipine-based regimen were more pronounced, especiall

108 We hypothesized that an amlodipine-based regimen would have more favorable effec

109 egimen: atenolol-based regimen, 7.9 +/- 1.8; amlodipine-based regimen, 8.8 +/- 2.0.

110 /- 17 mm Hg, diastolic BP of 82 +/- 9 mm Hg; amlodipine-based regimen, systolic BP of 136 +/- 15 mm H

111 Pressure Lowering Arm (ASCOT-BPLA) compared amlodipine-based regimens with atenolol-based regimens i

112 e was a reduction in TCVP in those allocated amlodipine-based therapy compared with atenolol-based th

113 the efficacy of atenolol-based compared with amlodipine-based therapy in patients with hypertension u

114 lowering with atenolol-based therapy versus amlodipine-based therapy in people with hypertension.

115 on in normal weight than obese patients, but amlodipine-based therapy is equally effective across BMI

116 ersus brand-name products for amlodipine and amlodipine-benazepril (HR [95% CI]: 0.91 [0.84-0.99] and

117 ite cardiovascular endpoint (for amlodipine, amlodipine-benazepril, and quinapril), non-vertebral fra

118 bjects prescribed dihydropyridines (excludes amlodipine) between 1995 and 2 years prior to the index

119 The amlodipine-bound structure reveals the molecular basis f

120 s and 1 favored AGs (patients switching from amlodipine brand-name: HR [95% CI] 0.92 [0.88-0.97]).

121 l and hydrochlorothiazide and benazepril and amlodipine, but rates were significantly lower with bena

122 g) with a combination such as aliskiren plus amlodipine can be recommended.

123 Amlodipine can increase CsA levels

124 Medications included chlorthalidone, amlodipine, carvedilol, cholecalciferol, erythropoietin,

125 In marked contrast, amlodipine caused a dose-dependent increase in nitrite p

126 Amlodipine causes increased blood flow and increased tim

127 ndividuals when comparing chlorthalidone and amlodipine (CHD: CC = 0.86; TC = 0.90; TT = 1.09; P = .0

128 The benazepril-amlodipine combination was superior to the benazepril-hy

129 Thus, in TM patients with cardiac siderosis, amlodipine combined with chelation therapy reduced cardi

130 ause of superior efficacy of benazepril plus amlodipine compared with benazepril plus hydrochlorothia

131 ing were attenuated in patients while taking amlodipine compared with ISMN.

132 ning a renin-angiotensin system blocker with amlodipine, compared with hydrochlorothiazide, was super

133 e-blind 20 or 40 mg fosinopril or 5 or 10 mg amlodipine daily for 4 weeks in a fixed-dose regimen.

134 Addition of bradykinin, enalaprilat, and amlodipine decreased oxygen consumption significantly le

135 Amlodipine did not increase cardiovascular morbidity or

136 exposed them to 4 different CCBs-nifedipine, amlodipine, diltiazem, and verapamil-at their physiologi

137 ry IVUS, which was repeated after 2 years of amlodipine, enalapril, or placebo therapy.

138 in response to agonist stimulation, whereas amlodipine enhanced P-selectin expression and atenolol i

139 083) while taking a calcium-channel blocker (amlodipine, felodipine, nifedipine, diltiazem, or verapa

140 omly assigned to 80 mg/d valsartan or 5 mg/d amlodipine for 24 weeks.

141 ted renal transplant patients were placed on amlodipine for an average of 6.9 wk and later withdrawn.

142 A 63-year-old male taking amlodipine for his hypertension presented with a 3-week

143 ospitals are routinely switching patients to amlodipine from other CCB for reasons of cost.

144 25.5 per 1000 patient-years) and 789 in the amlodipine group (10.4%, 24.7 per 1000 patient-years; ha

145 552 primary-outcome events in the benazepril-amlodipine group (9.6%) and 679 in the benazepril-hydroc

146 duced risk of the clinical end points vs the amlodipine group (95% confidence interval [CI], 20%-66%)

147 The lower risk of stroke in the amlodipine group (hazard ratio 0.78, 95% CI 0.67-0.90) w

148 l group (P = .08), and no progression in the amlodipine group (P = .31).

149 y, reduced variability in daytime SBP in the amlodipine group (p<0.0001) partly accounted for the red

150 nt lower in the irbesartan group than in the amlodipine group (P<0.001).

151 hereas there was a 0.0126-mm decrease in the amlodipine group (P:=0.007).

152 =0.02) and 23 percent lower than that in the amlodipine group (P=0.006).

153 .008) and 21 percent more slowly than in the amlodipine group (P=0.02).

154 ment were 131.6/73.3 mm Hg in the benazepril-amlodipine group and 132.5/74.4 mm Hg in the benazepril-

155 that variability decreased over time in the amlodipine group and increased in the atenolol group.

156 y disease progression in the benazepril plus amlodipine group compared with 215 (3.7%) in the benazep

157 PM variability in SBP were also lower in the amlodipine group than in the atenolol group (all p<0.000

158 lic blood pressure (SBP) SD was lower in the amlodipine group than in the atenolol group at all follo

159 ema was more frequent in the benazepril plus amlodipine group than in the benazepril plus hydrochloro

160 d less progression of atherosclerosis in the amlodipine group vs placebo (P = .12), with significantl

161 tients (14%) from the initial aliskiren plus amlodipine group, 45 (14%) from the aliskiren group, and

162 However, compared with the amlodipine group, after adjustment for baseline covariat

163 For the amlodipine group, correlation between blood pressure red

164 as compared with 33 percent of those in the amlodipine group, representing a 16 percent reduction in

165 t of the placebo group and 39 percent of the amlodipine group, representing a 9 percent reduction in

166 m the aliskiren group, and 58 (18%) from the amlodipine group.

167 rothiazide group than in the benazepril plus amlodipine group.

168 amin E (Group D) or 1% cholesterol diet plus amlodipine (Group E) for 12 weeks.

169 This report compares the ramipril and amlodipine groups following discontinuation of the amlod

170 The placebo and amlodipine groups had nearly identical average 36-month

171 However, compared with the metoprolol and amlodipine groups, the ramipril group manifested risk re

172 tical in the chlorthalidone, lisinopril, and amlodipine groups.

173 In contrast, amlodipine had a significant effect in slowing the 36-mo

174 Likewise, patients receiving amlodipine had a significantly lower rate of myocardial

175 Amlodipine has no demonstrable effect on angiographic pr

176 t few years a newer calcium channel blocker, amlodipine, has been used with increasing frequency.

177 The effect of a new CCB, amlodipine, has not been established.

178 % confidence interval, 0.94-1.15; P=0.46) or amlodipine (hazard ratio, 0.93; 95% confidence interval,

179 However, both AT1-receptor blockade and amlodipine improved in vivo left ventricular end-diastol

180 il significantly reduced PAI-1 compared with amlodipine in a dose-dependent fashion.

181 The beneficial effect of amlodipine in CHF may be due to a reduction of cytokines

182 determine whether the beneficial effects of amlodipine in heart failure may be mediated by a reducti

183 ce cardiac morbidity and mortality more than amlodipine in hypertensive patients at high cardiovascul

184 were significantly lower with benazepril and amlodipine in overweight patients (hazard ratio 0.76, 95

185 the use of valsartan (ARB) was compared with amlodipine in patients at high cardiovascular disease ri

186 valsartan lowered UAER more effectively than amlodipine in patients with type 2 diabetes and microalb

187 ve effect of chlorthalidone, lisinopril, and amlodipine in preventing HF.

188 the effect of a new calcium-channel blocker, amlodipine, in patients with severe chronic heart failur

189 CsA levels on amlodipine increased an average of 40% above baseline (P

190 to treat systemic hypertension and contains amlodipine, indapamide and perindopril arginine as activ

191 pine groups following discontinuation of the amlodipine intervention in September 2000.

192 -type calcium channel blocker, we found that amlodipine is able to activate Ca(2+) entry by enhancing

193 in an unbiased screen of 1650 compounds that amlodipine is able to inhibit survival of GBM cells by s

194 increased CsA levels after being changed to amlodipine is presented along with a prospective trial t

195 ested whether a combination of aliskiren and amlodipine is superior to each monotherapy in early cont

196 r second-generation dihydropyridines such as amlodipine, isradipine, nicardipine, and felodipine also

197 For amlodipine, IVUS showed evidence of slowing of atheroscl

198 rticipants were randomly assigned to receive amlodipine, lisinopril, or chlorthalidone.

199 9 participants randomized to chlorthalidone, amlodipine, lisinopril, or doxazosin treatments and foll

200 Attack Trial) determined that treatment with amlodipine, lisinopril, or doxazosin was not superior to

201 patients were randomized to chlorthalidone, amlodipine, lisinopril, or doxazosin, providing an oppor

202 done reduced the risk of HFPEF compared with amlodipine, lisinopril, or doxazosin; the hazard ratios

203 red in 29.2% of participants (chlorthalidone/amlodipine/lisinopril) with new-onset HFPEF versus 41.9%

204 Amlodipine lowers plasma IL-6 levels in patients with CH

205 ix cases have been published indicating that amlodipine may also promote gingival hyperplasia; howeve

206 that a portion of the beneficial actions of amlodipine may involve the release or action of NO.

207 Recent studies suggest that amlodipine may reduce mortality in patients with heart f

208 s, patients in the reduction group receiving amlodipine (n = 15) had a significant decrease in MIC co

209 who were lost to follow-up (benazepril plus amlodipine, n=70; benazepril plus hydrochlorothiazide, n

210 halidone; n = 13,860), a calcium antagonist (amlodipine; n = 8174), an angiotensin-converting enzyme

211 Neither amlodipine nor lisinopril is superior to chlorthalidone

212 The effect of amlodipine on cytokine levels in patients with CHF is un

213 eceive treatment with either benazepril plus amlodipine or benazepril plus hydrochlorothiazide.

214 prevalence of gingival overgrowth induced by amlodipine or diltiazem was not statistically significan

215 done reduced the risk of HFREF compared with amlodipine or doxazosin; the hazard ratios were 0.74 (95

216 HF risk decreased with chlorthalidone versus amlodipine or lisinopril use during year 1.

217 e appropriate model showed relative risks of amlodipine or lisinopril versus chlorthalidone during ye

218 isks (95% confidence intervals; P values) of amlodipine or lisinopril versus chlorthalidone were 1.35

219 .05; 95% CI, 0.77-1.42) than participants on amlodipine or lisinopril with incident diabetes (HR rang

220 channel blockers nifedipine, diltiazem, and amlodipine or the ACE inhibitors enalaprilat and ramipri

221 , a dihydropyridine calcium channel blocker (amlodipine) or a beta-blocker (metoprolol) as initial th

222 ic angina taking standard doses of atenolol, amlodipine, or diltiazem, without evident adverse, long-

223 Random assignment to chlorthalidone, amlodipine, or lisinopril.

224 effects of 7 days of treatment with placebo, amlodipine, or lisinopril.

225 d overt nephropathy treated with irbesartan, amlodipine, or placebo in addition to conventional antih

226 Patients were randomized to irbesartan, amlodipine, or placebo, with other antihypertensive agen

227 Treatment with irbesartan, amlodipine, or placebo.

228 essure were complete, created 5006 valsartan-amlodipine patient pairs matched exactly for systolic bl

229 g-regimens (atenolol+/-thiazide-based versus amlodipine+/-perindopril-based therapy) on derived centr

230 drug) to receive a daily regimen of 5 mg of amlodipine plus 12.5 mg of hydrochlorothiazide, 5 mg of

231 plus 12.5 mg of hydrochlorothiazide, 5 mg of amlodipine plus 4 mg of perindopril, or 4 mg of perindop

232 hat in black patients in sub-Saharan Africa, amlodipine plus either hydrochlorothiazide or perindopri

233 The difference between the group receiving amlodipine plus hydrochlorothiazide and the group receiv

234 at baseline and at 6 months, those receiving amlodipine plus hydrochlorothiazide and those receiving

235 plus hydrochlorothiazide and those receiving amlodipine plus perindopril had a lower 24-hour ambulato

236 hydrochlorothiazide and the group receiving amlodipine plus perindopril was -0.14 mm Hg (95% CI, -2.

237 ent with 150 mg aliskiren plus placebo, 5 mg amlodipine plus placebo, or 150 mg aliskiren plus 5 mg a

238 In in vitro experiments, both lovastatin and amlodipine preserved SOD activity and reduced the oxidiz

239 mented diet and by N-acetylcysteine, whereas amlodipine prevented Ca2+ loading and an altered redox s

240 The possibility that amlodipine prolongs survival in patients with nonischemi

241 atio, 0.72 [CI, 0.52 to 1.00]; P = 0.048) or amlodipine recipients (hazard ratio, 0.65 [CI, 0.48 to 0

242 uctions in central aortic pressures with the amlodipine regimen (central aortic systolic BP, Delta4.3

243 Thus, unlike nifedipine and diltiazem, amlodipine releases NO from blood vessels.

244 ose individuals taking chlorthalidone versus amlodipine remained decreased but less so, whereas it wa

245 oregulation impairment (3/4 nephrectomy plus amlodipine), renal blood flow in conscious animals (but

246 Ramipril, compared with amlodipine, retards renal disease progression in patient

247 ihypertensive treatment with benazepril plus amlodipine should be considered in preference to benazep

248 Bradykinin, enalaprilat, and amlodipine significantly suppressed cortical oxygen cons

249 er irbesartan or the calcium-channel blocker amlodipine slows the progression of nephropathy in patie

250 defects in responsiveness to enalaprilat and amlodipine, suggesting that inactivation of NO by supero

251 In the Prospective Randomized Amlodipine Survival Evaluation (PRAISE) trial, we used e

252 nical trials (PRAISE [Prospective Randomized Amlodipine Survival Evaluation], PRAISE-2, MERIT-HF [Met

253 We analyzed data from Prospective Randomized Amlodipine Survival Trial (PRAISE).

254 pill antihypertensive therapy (consisting of amlodipine, telmisartan, and chlorthalidone) than in tho

255 eriod (blood pressure 4.0/2.1 mm Hg lower in amlodipine than valsartan group after 1 month; 1.5/1.3 m

256 However, in those allocated benazepril and amlodipine, the primary endpoint did not differ between

257 g an absolute risk reduction with benazepril-amlodipine therapy of 2.2% and a relative risk reduction

258 ut inequalities in blood pressure, favouring amlodipine, throughout the multiyear trial precluded com

259 We evaluated whether addition of amlodipine to chelation strategies would reduce myocardi

260 Administration of amlodipine to patients with CAD and normal blood pressur

261 the ability of bradykinin, enalaprilat, and amlodipine to suppress oxygen consumption in tissue from

262 ar systolic pressure in the AT1-blocker- and amlodipine-treated LVH groups (189 +/- 9 and 188 +/- 16

263 1%) placebo-treated patients, in 110 (16.6%) amlodipine-treated patients (hazard ratio [HR], 0.69; 95

264 AT1-blocker-treated (11.0 +/- 1.7 mm Hg) and amlodipine-treated rats (11.5 +/- 1.8 mm Hg) and was sim

265 zed in both the AT1-blocker-treated rats and amlodipine-treated rats.

266 ectively, both P<0.05) and were reduced with amlodipine treatment (2108+/-199 and 480+/-74, respectiv

267 +/-2, P<0.05) and increased with concomitant amlodipine treatment (29+/-2, P<0.05).

268 +/-1, P<0.05) and was increased with chronic amlodipine treatment (52+/-1, P<0.05).

269 rsus 3.1+/-0.3, P<0.05) and was reduced with amlodipine treatment (6.6+/-1.1, P<0.5).

270 lower after lisinopril treatment than after amlodipine treatment (P = .03).

271 Amlodipine treatment did not cause any serious adverse e

272 Chronic amlodipine treatment in this model of developing CHF pro

273 Neither amlodipine treatment nor aspirin or warfarin use altered

274 w during treadmill exercise, whereas chronic amlodipine treatment normalized LV stroke volume and imp

275 This study examined the effects of chronic amlodipine treatment on left ventricular (LV) pump funct

276 scular resistance was lower (P = .016) after amlodipine treatment than after lisinopril treatment.

277 Amlodipine treatment was associated with reduced cardiov

278 reduced by 50% from CHF values with chronic amlodipine treatment.

279 ity or major cardiovascular events, although amlodipine use was associated with fewer cases of unstab

280 IVUS) substudy of the CAMELOT (Comparison of Amlodipine Versus Enalapril to Limit Occurrences of Thro

281 y lower at 26 weeks in patients treated with amlodipine versus placebo (p = 0.007 by the Wilcoxon sig

282 a decrease in strokes in patients receiving amlodipine versus those receiving placebo (hazard ratio,

283 Other outcomes included comparisons of amlodipine vs enalapril and enalapril vs placebo.

284 s usual BP goal; ramipril vs metoprolol; and amlodipine vs metoprolol.

285 r was incidence of cardiovascular events for amlodipine vs placebo.

286 rimary end point comparison for enalapril vs amlodipine was not significant (HR, 0.81; 95% CI, 0.63-1

287 Amlodipine was similar to chlorthalidone in reducing CHD

288 ntihypertensive therapy with benazepril plus amlodipine was superior to benazepril plus hydrochloroth

289 Amlodipine was the most commonly prescribed calcium-chan

290 and decreased to baseline (P = 0.001) after amlodipine was withdrawn, despite no significant change

291 odipine, and 617 allocated to aliskiren plus amlodipine were available for analysis.

292 gnificant differences between fosinopril and amlodipine were found for short-term changes in tissue p

293 odipine, whereas the effects of atenolol and amlodipine were not additive.

294 GTN neutralized the proactivatory effects of amlodipine, whereas the effects of atenolol and amlodipi

295 in the groups given lovastatin, vitamin E or amlodipine with a high cholesterol diet.

296 ly in rabbits given lovastatin, vitamin E or amlodipine with a high cholesterol diet.

297 lence of overgrowth induced by diltiazem and amlodipine, with estimates of 74% and 3.3%, respectively

298 Amlodipine, with its intrinsically long half-life alone

299 od pressures, regimens based on valsartan or amlodipine would have differing effects on cardiovascula

300 A secondary hypothesis was whether amlodipine would reduce the rate of atherosclerosis in t

301 sked clinical trial designed to test whether amlodipine would slow the progression of early coronary