ライフサイエンスコーパス: candesartan

1 and angiotensin receptor blockers (losartan, candesartan).

2 uced (-60%) at 10-15 min after blockade with candesartan.

3 by co-infusion with AT1 receptor antagonist, candesartan.

4 bited by PD98059 and AT1 receptor antagonist candesartan.

5 orothioate oligomers but not by 10(-6) mol/L candesartan.

6 not inhibited by AT1 receptor blockade using candesartan.

7 hypertensive effects of the AT(1) antagonist Candesartan.

8 ters perfusion pressure that were reduced by candesartan.

9 coadministration of the AT1 receptor blocker candesartan.

10 ortical actin fibres and this was blocked by candesartan.

11 was ameliorated 30 days after injury only by candesartan.

12 t or to all of the neuroprotective effect of candesartan.

13 h-dose losartan against the highest doses of candesartan.

14 ction fraction were randomized to placebo or candesartan.

15 Peripherally administered Candesartan (0.1, 0.5 or 1.0 mg/kg per day) inhibits AT(

16 ensin II receptor type 1 was inhibited using candesartan (0.1, 0.5, 1 mg/kg) after trauma to determin

17 ted HR for good adherence was similar in the candesartan (0.66, 0.55-0.81, p<0.0001) and placebo (0.6

18 The highest dose of candesartan (1 mg/kg) elicited rapid reductions in arter

19 Sprague-Dawley rats were pretreated with candesartan (10 mg x kg(-1) x d(-1)) for 2 weeks and stu

20 type 1 angiotensin II (AT1) receptor blocker candesartan (10 mg/kg) to untreated control mice increas

21 t PET imaging, blocking with AT1R antagonist candesartan (10 mg/kg), and plasma metabolism analysis w

22 master muscle arterioles the AT1 R inhibitor candesartan (10(-7) -10(-5) m) showed partial but concen

23 n of the AngII type 1 (AT1) receptor blocker candesartan (10(-8) M).

24 oglia activation (vehicle: 163 +/- 25/mm vs. candesartan: 118 +/- 13/mm).

25 ed to DIRECT-Protect 1, and were assigned to candesartan 16 mg once a day or matching placebo.

26 suvastatin (10 mg per day) or placebo and to candesartan (16 mg per day) plus hydrochlorothiazide (12

27 combination of rosuvastatin (10 mg per day), candesartan (16 mg per day), and hydrochlorothiazide (12

28 Compared with high doses of candesartan (16-32 mg), low-dose (12.5 mg) and medium-do

29 In rats not treated with candesartan, 24 h isolation stress increased pituitary A

30 The effects of candesartan (30 microg/kg i.v.) and PD123319 (10 mg/kg i

31 ug discontinuation rates were similar in the candesartan (30%) and placebo (29%) groups.

32 A total of 78 weeks of candesartan (32 mg/d) or placebo treatment; study treatm

33 mortality also was significantly reduced by candesartan (642 [28.0%] versus 708 [31.0%]; HR 0.88 [95

34 mined the effect of subcutaneous infusion of candesartan, a non-competitive AT(1) receptor antagonist

35 Reactivity to AngII before and during candesartan administration was assessed by measuring (by

36 Daily treatment with candesartan afforded sustained reduction of brain damage

37 ly reduced some of the beneficial effects of candesartan after CCI, suggesting that PPARgamma activat

38 We aimed to find out whether candesartan, an angiotensin-receptor blocker, could impr

39 Candesartan, an inverse agonist of the type 1 angiotensi

40 e determined in 4576 low LVEF patients (2289 candesartan and 2287 placebo), titrated as tolerated to

41 3.5 percent of the participants assigned to candesartan and 5.9 percent of those receiving placebo.

42 886 (23%) patients in the candesartan and 945 (25%) in the placebo group died (una

43 A expression by 2-fold, which was blocked by candesartan and a general PKC inhibitor, GF109203X.

44 cardiac fibrosis were partially inhibited by candesartan and benazepril, whereas aliskiren produced c

45 Candesartan and EXP3174 are competitive, reversible insu

46 +/-1.0 to 22.9+/-1.1 ml/d in rats given only candesartan and from 11.5+/-0.7 to 22.0+/-0.6 ml/d in ra

47 effects of the AT1 and AT2 receptor blockers candesartan and PD123319 on hemodynamic responses to ang

48 Both candesartan and PKC inhibition caused increased G-actin

49 ation between adherence and mortality in the candesartan and placebo groups.

50 Both candesartan and telmisartan ameliorated controlled corti

51 The neurorestorative effects of candesartan and telmisartan were reduced by concomitant

52 matic brain injury, we selected two sartans, candesartan and telmisartan, of proven therapeutic effic

53 ct injury, we determined effective doses for candesartan and telmisartan, their therapeutic window, m

54 However, candesartan and valsartan were the most potent at blocki

55 AT1 receptor blockade (candesartan) and ACE inhibition (trandolapril) were also

56 f 409 participants were randomly assigned to candesartan, and 400 to placebo.

57 because AT1 receptor antagonists valsartan, candesartan, and losartan inhibited Ang II-induced endog

58 een pretreated (for 30 min) with intravenous candesartan, AngII-induced renal vasoconstriction was in

59 Treatment of prehypertension with candesartan appeared to be well tolerated and reduced th

60 giotensin converting enzyme receptor blocker candesartan appears to be effective and highly tolerable

61 Diabetic rats were treated with insulin, candesartan (ARB), benazepril (ACE inhibitor), or aliski

62 Thirteen rabbits received candesartan at 0.5 mg x kg(-1) x d(-1) beginning 2 days

63 Candesartan at 1 mg/kg per d prevented any increase in a

64 In the two groups of rats receiving candesartan at 10 mg/kg per d (with and without ibuprofe

65 Therapy with candesartan at a dose of 16 mg per day plus hydrochlorot

66 ave cardiovascular disease to receive either candesartan at a dose of 16 mg per day plus hydrochlorot

67 rectomy and were given vehicle (control), or candesartan at a standard 5 mg/kg per d (T5), high 25 mg

68 All patients were randomized to candesartan at a target dose of 32 mg once daily or matc

69 and had no effect on the changes produced by candesartan at either dose.

70 re randomly assigned to receive two years of candesartan (Atacand, AstraZeneca) or placebo, followed

71 Treatment with 0.01 mg/kg candesartan attenuated the arterial pressure responses b

72 s well as the specific AT1R blocker CV11974 (candesartan) attenuated the cell-injurious effects of ox

73 Pretreatment with candesartan before an acute MI improves global LV functi

74 Coadministration of candesartan blocked AngII effects in a dose-dependent ma

75 ressor responses to AngII were attenuated by candesartan but were not altered by PD123319.

76 es and microglia during EAE was blocked with candesartan (CA), an inhibitor of AT1R.

77 angiotensin II type 1 receptor blocker (ARB) candesartan can reduce the risk of stroke in elderly pat

78 RRM + ramipril (Ram, 10 mg/kg per d), RRM + candesartan (Can, 10 mg/kg per d), or sham surgery.

79 ups derive incremental clinical benefit from candesartan, careful surveillance of serum potassium and

80 < 0.05 versus untreated); however, high-dose candesartan caused a significant increase in renal damag

81 Concurrent injection of candesartan caused dose-dependent inhibition of AngII up

82 rafenib) or low micromolar range (abiratone, candesartan, celecoxib, dasatinib, nilvadipine, nimodipi

83 rats received the novel AT1 receptor blocker candesartan cilexetil (1.0 mg/kg per d) in the drinking

84 lowing during a 2-wk treatment protocol: (1) candesartan cilexetil (AT1 receptor antagonist) at 1 mg/

85 Candesartan cilexetil administration prevented the AngII

86 ofen at 30 mg/kg per d; (4) a combination of candesartan cilexetil at 1 mg/kg per d + ibuprofen; (5)

87 cilexetil at 1 mg/kg per d + ibuprofen; (5) candesartan cilexetil at 10 mg/kg per d + ibuprofen; and

88 or antagonist) at 1 mg/kg body wt per d; (2) candesartan cilexetil at 10 mg/kg per d; (3) ibuprofen a

89 urthermore, inhibition of AT1 receptors with candesartan cilexetil provides protection against AngII-

90 Both low- and high-dose candesartan cilexetil significantly reduced cardiac and

91 rats and to determine the effect of chronic candesartan cilexetil treatment on autoregulatory behavi

92 o 4.9 micromol/kg) antihypertensive doses of candesartan cilexetil were initiated after hypertension

93 In animals receiving AngII + candesartan cilexetil, stepwise changes in perfusion pre

94 Trials (DIRECT) Programme to assess whether candesartan could reduce the incidence and progression o

95 ether the angiotensin-receptor blocker (ARB) candesartan decreases cardiovascular mortality, morbidit

96 Candesartan did not affect changes in NT-proBNP and hs-T

97 Treatment with candesartan did not reduce or prevent the development of

98 Conversely, peripheral treatment with Candesartan does not affect AT(1A) receptor mRNA, the pr

99 The lower candesartan dose, which did not cause hypotension, elici

100 In addition, Candesartan dose-dependently decreases AT(1) binding in

101 trictor responses to AngII were abolished by candesartan doses of 1 and 0.1 mg/kg.

102 Treatment with candesartan during Ang II-induced hypertension attenuate

103 Candesartan effectively blocks AT1A and AT1B receptors i

104 sin II (AngII) type 1 (AT1) receptor blocker candesartan elicited divergent renal hemodynamic and exc

105 by single and daily repeated treatment with candesartan for 5 days after controlled cortical impact.

106 Thus, candesartan given before an MI attenuates LV remodeling

107 f 20 fatal/non-fatal strokes occurred in the candesartan group (7.2/1,000 patient-years) and 35 in th

108 49 years; age range, 25-69 years) 103 in the candesartan group (mean age, 50 years; age range, 25-69

109 in the placebo group and 208 of those in the candesartan group (relative risk reduction, 15.6 percent

110 in the placebo group and 53 of those in the candesartan group (relative risk reduction, 66.3 percent

111 c events was 0.28 (95% CI, 0.13-0.40) in the candesartan group and 0.16 (95% CI, 0.08-0.22) in the pl

112 adverse effects by 23.1% of patients in the candesartan group and 18.8% in the placebo group; the re

113 Data on 772 participants (391 in the candesartan group and 381 in the placebo group; mean age

114 .7 months, 334 (33%) of 1013 patients in the candesartan group and 406 (40%) of 1015 in the placebo g

115 483 (38%) patients in the candesartan group and 538 (42%) in the placebo group exp

116 the ISH patients, 754 were randomized to the candesartan group and 764 to the control group.

117 od pressure was reduced by 22/6 mm Hg in the candesartan group and by 20/5 mm Hg in the control group

118 Both the candesartan group and the placebo group were instructed

119 There were 3.8% more cardiac events in the candesartan group than in the placebo group (95% CI, -7%

120 hy occurred in 127 (13%) participants in the candesartan group versus 124 (13%) in the placebo group.

121 hy was seen in 178 (25%) participants in the candesartan group versus 217 (31%) in the placebo group.

122 Of the patients in the candesartan group, 817 (35.7%) experienced cardiovascula

123 HF (757 [20%] vs 918 [24%], p<0.0001) in the candesartan group.

124 Candesartan had no effect on LV tissue endothelial nitri

125 These findings suggest that candesartan has dosage-dependent, anti-inflammatory effe

126 11.5+/-0.7 to 22.0+/-0.6 ml/d in rats given candesartan + ibuprofen.

127 The candesartan IC50 values for percentage changes in renal

128 Candesartan in a dose of 3 microg/kg intravenously (i.v.

129 ecific mortality in patients enrolled in the Candesartan in Heart failure Assessment of Reduction in

130 VEF, a prespecified analysis of the combined Candesartan in Heart Failure Assessment of Reduction in

131 ed systolic function trial (I-Preserve), the Candesartan in Heart failure Assessment of Reduction in

132 [The Health Improvement Network], and CHARM [Candesartan in Heart Failure-Assessment of Reduction in

133 Participants in the CHARM (Candesartan in Heart Failure-Assessment of Reduction in

134 rtery Catheterization Effectiveness], CHARM [Candesartan in Heart Failure: Assessment of Reduction in

135 adherence and clinical outcome in the CHARM (Candesartan in Heart failure: Assessment of Reduction in

136 of symptomatic heart failure enrolled in the Candesartan in Heart failure: Assessment of Reduction in

137 iovascular (CV) versus non-CV reasons in the Candesartan in Heart Failure: Assessment of Reduction in

138 Patients enrolled in the CHARM (Candesartan in Heart failure: Assessment of Reduction in

139 s Investigation Group) trials and the CHARM (Candesartan in Heart Failure: Assessment of Reduction in

140 and during follow-up of 2310 patients in the Candesartan in Heart failure: Assessment of Reduction in

141 lure patients from the North American CHARM (Candesartan in Heart Failure: Assessment of Reduction in

142 in 2400 women and 5199 men randomized in the Candesartan in Heart failure: Assessment of Reduction in

143 We used data from the Candesartan in Heart failure: Assessment of Reduction in

144 icular ejection fractions (mean, 39%) in the Candesartan in Heart failure: Assessment of Reduction in

145 HF hospitalization and randomization in the Candesartan in Heart failure: Reduction in Mortality and

146 To evaluate the responses to candesartan in hypertensive rats, experiments were perfo

147 The benefit of candesartan in reducing cardiovascular death or heart fa

148 The effect of candesartan in reducing cardiovascular outcomes was cons

149 The effect of candesartan in reducing outcomes was independent of hemo

150 inhibited by 88% by the AT1 receptor blocker candesartan in renal SMC.

151 hereas the exacerbation of renal injury with candesartan in the Dahl salt-sensitive model was inverse

152 stingly, the beneficial end-organ effects of candesartan in the nitric oxide synthase inhibition mode

153 iotensin II type 1 receptor (AT1) antagonist candesartan increased renal insulin receptor expression

154 Candesartan increased the rate of aggregate hyperkalemia

155 Candesartan increased the steady-state autoregulatory in

156 ) were similar in the absence or presence of candesartan, indicating that AT1 R-mediated myogenic con

157 s study documents AT1-dependent enhancement (candesartan-inhibitable) of bicarbonate reabsorption and

158 nt of metanephroi with the AT(1)R antagonist candesartan inhibited UB branching, decreasing the numbe

159 Q257A mutant, the dissociation rate of [(3)H]candesartan is 2.8-fold more than the rate observed with

160 These results indicate that candesartan is a potent and selective angiotensin AT1 re

161 These studies establish that candesartan is an effective, highly selective, AT1 recep

162 These results indicate that candesartan is neuroprotective, reducing neuronal injury

163 the Q257A mutant pretreated with EXP3174 and candesartan is surmountable.

164 The 0.1 mg/kg dose of candesartan led to gradual reductions in arterial pressu

165 Compared with candesartan, losartan was not associated with increased

166 pared with untreated rats, pretreatment with candesartan lowered (P<0.05) LV systolic pressure and th

167 At a dose of 10 mg/kg per d, candesartan lowered arterial pressure from 131+/-2 to 91

168 We randomly assigned patients candesartan (n=1276, target dose 32 mg once daily) or pl

169 ents (7599 with data) were randomly assigned candesartan (n=3803, titrated to 32 mg once daily) or ma

170 (aged 18-50 years) were randomly assigned to candesartan (n=711) or to placebo (n=710) in DIRECT-Prev

171 CT-Prevent 1, and 1905 (aged 18-55 years) to candesartan (n=951) or to placebo (n=954) in DIRECT-Prot

172 Except for candesartan, no drugs have been tested in randomized cli

173 Neither candesartan nor PD123319 had a significant effect on bas

174 We assessed the effect of candesartan on cause-specific mortality in patients enro

175 e the efficacy of octreotide, celecoxib, and candesartan on DR.

176 sin II (AngII) type I (AT1) receptor blocker candesartan on renal vascular reactivity in vivo.

177 angiotensin II (AngII) AT1 receptor blocker candesartan on responses to AngII were investigated in t

178 he inhibitory effects of the larger doses of candesartan on responses to AngII were long in duration,

179 blockade of angiotensin II AT1 receptors by candesartan on the exaggerated tubuloglomerular feedback

180 dosages of the angiotensin receptor blocker candesartan on the progression of renal injury in sponta

181 Ang II receptor type 1 blocker candesartan or ACE inhibitor captopril markedly attenuat

182 enuded diabetic aortas but was attenuated by candesartan or captopril, indicating that NOX remains ac

183 iabetic aortas but significantly restored by candesartan or captopril.

184 AT(1) receptor blockade with candesartan or losartan (10(-6) M) prevented the stimula

185 with an LVEF of < or =40% were randomized to candesartan or placebo in 2 complementary parallel trial

186 years were randomly assigned to double-blind candesartan or placebo with open-label antihypertensive

187 mized to standard heart failure therapy plus candesartan or placebo, titrated as tolerated to a targe

188 We administered candesartan or vehicle to mice 5 h before CCI injury.

189 associated with death reported in 2 (0.05%) candesartan patients and 1 (0.03%) placebo patient.

190 With candesartan pretreatment, LV fractional shortening and e

191 RNA and content in the PVN were prevented by candesartan pretreatment, suggesting that activation of

192 pport the hypothesis that concomitant use of candesartan protects against a decrease in left ventricu

193 Candesartan reduced both sudden death (HR 0.85 [0.73 to

194 Candesartan reduced each of the components of the primar

195 Candesartan reduced sudden death and death from worsenin

196 Acute AT1 receptor blockade by candesartan reduced tubuloglomerular feedback responses

197 Although candesartan reduces the incidence of retinopathy, we did

198 antihypertensive treatment based on the ARB candesartan resulted in a significant 42% RR reduction i

199 There was no significant heterogeneity for candesartan results across the component trials.

200 hypertension was reduced using captopril or candesartan, retinal KDR expression returned to baseline

201 nistered the insurmountable AT(1) antagonist Candesartan, s.c. via osmotic minipumps for 14 days, to

202 At doses of 30 and 300 microg/kg i.v., candesartan shifted the dose-response curve to AngII to

203 ACEI captopril and quinaprilate and the ARB candesartan significantly increased plasma renin concent

204 Candesartan significantly reduces all-cause mortality, c

205 rdiac myocytes, which were not normalized by candesartan, suggesting that Ang II was synthesized intr

206 Patients were randomly assigned candesartan (target dose 32 mg once daily) or matching p

207 More patients discontinued candesartan than placebo because of concerns about renal

208 ng generic users of losartan, valsartan, and candesartan, there was an increase in rates of adverse e

209 Patients were randomized to candesartan, titrated to 32 mg QD, or placebo and were f

210 The addition of candesartan to ACE inhibitor and other treatment leads t

211 e of an angiotensin type 1 receptor blocker, candesartan, to normalize aldosterone production to cont

212 Candesartan-treated mice also showed better motor skills

213 Candesartan-treated rabbits had less atherosclerosis (in

214 was abolished by ramipril (1.40+/-0.13) and candesartan treatment (1.56+/-0.11).

215 th sham-operated rats (1.38+/-0.06) and that candesartan treatment caused a further decrease in renal

216 level was more likely to have improved with candesartan treatment in both DIRECT-Prevent 1 (odds 1.1

217 Candesartan treatment reduced the lesion volume after CC

218 crease in turning point to 18.0 nl/min after candesartan treatment.

219 spective cohorts of the DIabetic REtinopathy Candesartan Trial (DIRECT): PROTECT-1 and PREVENT-1.

220 therefore designed the DIabetic REtinopathy Candesartan Trials (DIRECT) Programme to assess whether

221 during 3675 person-years among 2082 users of candesartan (unadjusted IR/100 person-years, 9.0; 95% CI

222 adverse events for losartan, valsartan, and candesartan users (N=136 177) aged >/=66 years were calc

223 Hazard ratio (HR for candesartan vs placebo) was 0.82 (95% CI 0.67-1.00, p=0.

224 igh tolerability of the AT1 receptor blocker candesartan warrants further studies to assess its role

225 In contrast, when candesartan was administered at 0.01 mg/kg, a dose that

226 Candesartan was administered into the renal artery of no

227 heterogeneity for the beneficial effects of candesartan was found across prespecified and subsequent

228 Candesartan was generally well tolerated and reduced car

229 Candesartan was generally well tolerated and significant

230 ilure, overall use of losartan compared with candesartan was not associated with an increased mortali

231 Candesartan was without effect on vasoconstrictor respon

232 Ang II receptor blockade, the AT(1) blocker, candesartan, was orally administered to spontaneously hy

233 The inhibitory effects of candesartan were insurmountable, and a vasodepressor or

234 New users of losartan and candesartan were selected for inclusion in the study coh

235 The benefits of candesartan were similar in all predefined subgroups, in

236 dly attenuated by systemic administration of candesartan, whereas TGF was basically unchanged in euvo

237 ent of sustained antihypertensive actions of candesartan, whereas the exacerbation of renal injury wi

238 ieved by intravenous injection of 0.05 mg/kg candesartan, which did not affect mean arterial pressure

239 Increases were more pronounced for generic candesartan, which is the studied product with the large

240 erol (OAG) reversed the inhibitory effect of candesartan, while this rescue effect was prevented by t

241 effects of the angiotensin receptor blocker candesartan with placebo in 7599 patients with CHF.

242 ind, controlled, clinical trials we compared candesartan with placebo in three distinct populations.

243 ngiotensin II receptor type 1 with 0.1 mg/kg candesartan within 4 hrs of injury significantly reduced

244 njury on mice to investigate whether the ARB candesartan would mitigate any effects of TBI.