ライフサイエンスコーパス: candesartan

1 and angiotensin receptor blockers (losartan, candesartan).

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

3 bited by PD98059 and AT1 receptor antagonist candesartan.

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

5 not inhibited by AT1 receptor blockade using candesartan.

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

7 ters perfusion pressure that were reduced by candesartan.

8 uced (-60%) at 10-15 min after blockade with 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 range, 21 to 28 months) after randomization (candesartan, 1.7% [95% CI, 0.5 to 2.8]; no candesartan,

20 (candesartan, 1.7% [95% CI, 0.5 to 2.8]; no candesartan, 1.8% [95% CI, 0.6 to 3.0]; metoprolol, 1.6%

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

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

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

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

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

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

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

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

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

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

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

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

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

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

35 after acute intrarenal arterial infusion of candesartan (4.2 mug kg(-1) ) or intravenous infusion of

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

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

38 tional analysis showed that RAS blockade via candesartan abolished microglial-induced capillary const

39 The AT(1)R blockers irbesartan and candesartan abrogated antifibrotic signal transduction o

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

41 Daily treatment with candesartan afforded sustained reduction of brain damage

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

43 Candesartan also ameliorated serelaxin's antifibrotic ac

44 ated cognitive impairment, we tested whether candesartan, an angiotensin II type 1 receptor (AT1R) an

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

46 Candesartan, an inverse agonist of the type 1 angiotensi

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

48 3.5 percent of the participants assigned to candesartan and 5.9 percent of those receiving placebo.

49 886 (23%) patients in the candesartan and 945 (25%) in the placebo group died (una

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

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

52 Combination candesartan and carvedilol therapy had no demonstrable c

53 domized to standard of care plus combination candesartan and carvedilol therapy or standard of care a

54 r troponin-guided treatment with combination candesartan and carvedilol therapy prevents the developm

55 Candesartan and EXP3174 are competitive, reversible insu

56 +/-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

57 re excluded for the choices of lisinopril vs candesartan and hydrochlorothiazide vs amlodipine.

58 udy aimed to assess the long-term effects of candesartan and metoprolol or their combination to preve

59 angiotensin II AT(1) receptor blockade using candesartan and mineralocorticoid receptor blockade usin

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

61 Both candesartan and PKC inhibition caused increased G-actin

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

63 Both candesartan and telmisartan ameliorated controlled corti

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

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

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

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

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

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

70 tensin receptor blocker such as enalapril or candesartan, and a calcium channel blocker such as amlod

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

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

73 l [angiotensin-converting enzyme inhibitor], candesartan [angiotensin-receptor blocker], hydrochlorot

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

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

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

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

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

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

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

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

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

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

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

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

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

87 atment with the angiotensin receptor blocker candesartan attenuated the reduction in left ventricular

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

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

90 teric site near the WPD loop of PRL-3, while Candesartan binds a potentially novel targetable site ad

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

92 Candesartan blocked cancer-induced spatial memory impair

93 broad-spectrum PRL inhibitors, Salirasib and Candesartan, blocked PRL-3-induced migration in human em

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

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

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

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

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

99 < 0.05 versus untreated); however, high-dose candesartan caused a significant increase in renal damag

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

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

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

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

104 Candesartan cilexetil administration prevented the AngII

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

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

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

108 ved Systolic Function], and CHARM Preserved [Candesartan Cilexetil in Heart Failure Assessment of Red

109 Systolic Function [I-PRESERVE]; NCT00095238; Candesartan Cilexetil in Heart Failure Assessment of Red

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

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

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

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

114 were assigned to concomitant treatment with candesartan cilexetil, metoprolol succinate, or matching

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

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

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

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

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

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

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

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

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

124 Candesartan during adjuvant therapy did not prevent redu

125 Treatment with candesartan during Ang II-induced hypertension attenuate

126 Candesartan effectively blocks AT1A and AT1B receptors i

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

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

129 Thus, candesartan given before an MI attenuates LV remodeling

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

131 49 years; age range, 25-69 years) 103 in the candesartan group (mean age, 50 years; age range, 25-69

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

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

134 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

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

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

137 .7 months, 334 (33%) of 1013 patients in the candesartan group and 406 (40%) of 1015 in the placebo g

138 483 (38%) patients in the candesartan group and 538 (42%) in the placebo group exp

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

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

141 Both the candesartan group and the placebo group were instructed

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

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

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

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

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

147 Candesartan had no effect on LV tissue endothelial nitri

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

149 11.5+/-0.7 to 22.0+/-0.6 ml/d in rats given candesartan + ibuprofen.

150 The candesartan IC50 values for percentage changes in renal

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

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

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

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

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

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

157 g of patients with HF was conducted from the Candesartan in Heart Failure-Assessment of Reduction in

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

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

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

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

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

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

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

165 en and 4010 men enrolled in CHARM-Preserved (Candesartan in Heart failure: Assessment of Reduction in

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

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

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

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

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

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

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

173 The effect of candesartan in reducing cardiovascular outcomes was cons

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

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

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

177 xygen tension increased in both groups after candesartan in the low Na(+) group.

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

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

180 Candesartan increased the rate of aggregate hyperkalemia

181 Candesartan increased the steady-state autoregulatory in

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

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

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

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

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

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

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

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

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

191 d 11 drugs (captopril, enalapril, valsartan, candesartan, long-acting metoprolol succinate, bisoprolo

192 Compared with candesartan, losartan was not associated with increased

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

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

195 Candesartan lowered tumour necrosis factor (Tnf) express

196 We provide the first evidence that candesartan may offer a low-cost strategy to prevent can

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

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

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

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

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

202 Neither candesartan nor CAP affected arterial pressure.

203 Neither candesartan nor PD123319 had a significant effect on bas

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

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

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

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

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

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

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

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

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

213 iabetic aortas but significantly restored by candesartan or captopril.

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

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

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

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

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

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

220 With candesartan pretreatment, LV fractional shortening and e

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

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

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

224 Candesartan reduced each of the components of the primar

225 Candesartan reduced SBP by -6.56 mm Hg (P < .001; n = 24

226 Candesartan reduced sudden death and death from worsenin

227 Acute AT1 receptor blockade by candesartan reduced tubuloglomerular feedback responses

228 Although candesartan reduces the incidence of retinopathy, we did

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

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

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

232 Candesartan's efficacy was associated with reduced hippo

233 of mice with cardiomyopathy, indicating that candesartan's inhibitory effects were not confined to th

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

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

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

237 Candesartan significantly reduces all-cause mortality, c

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

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

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

241 cardioprotection (combination carvedilol and candesartan therapy) or standard care alone.

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

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

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

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

246 Candesartan-treated mice also showed better motor skills

247 Candesartan-treated rabbits had less atherosclerosis (in

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

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

250 Candesartan treatment during adjuvant therapy was associ

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

252 Candesartan treatment reduced the lesion volume after CC

253 While candesartan treatment reversed capillary constriction in

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

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

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

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

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

259 ine, candesartan vs hydrochlorothiazide, and candesartan vs amlodipine.

260 drochlorothiazide, lisinopril vs amlodipine, candesartan vs hydrochlorothiazide, and candesartan vs a

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

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

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

264 Candesartan was administered into the renal artery of no

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

266 Candesartan was generally well tolerated and reduced car

267 Candesartan was generally well tolerated and significant

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

269 Candesartan was without effect on vasoconstrictor respon

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

271 Nifedipine and candesartan were also found by signal detection methods

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

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

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

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

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

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

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

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

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

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

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

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