ライフサイエンスコーパス: losartan

1 ty to the angiotensin receptor blocker (ARB) losartan.

2 pressor response of 25.5 mg/kg) relative to losartan.

3 mized to daily receive losartan 100 mg or no losartan.

4 he angiotensin II type 1 receptor antagonist losartan.

5 the Ang II type 1 (AT1) receptor antagonist losartan.

6 levels and these effects were not blocked by losartan.

7 ment with the Ang II type 1 receptor blocker losartan.

8 lar hyperpermeability; all were inhibited by losartan.

9 ith the addition of either spironolactone or losartan.

10 , +10.5%, P = 0.20) in the group assigned to losartan.

11 ntions were used; isoflurane anaesthesia and losartan.

12 ial that assessed renoprotective efficacy of losartan.

13 losartan, 1.8+/-1.5 mm/3 years, n=21 versus losartan 0.5+/-0.8 mm/3 years, n=17; P=0.001) and not in

14 losartan, 1.2+/-1.7 mm/3 years, n=38 versus losartan 0.8+/-1.3 mm/3 years, n=41; P=0.197).

15 losartan, 1.3+/-1.5 mm/3 years, n=59 versus losartan, 0.8+/-1.4 mm/3 years, n=58; P=0.009).

16 versus Ang II); adding the AT(1) antagonist losartan (1 microm) resulted in Ang II stimulating NO by

17 Further, the AT1 R blocker losartan (1 mum) diminished myogenic tone and blocked st

18 1) and not in dominant negative patients (no losartan, 1.2+/-1.7 mm/3 years, n=38 versus losartan 0.8

19 ntly reduced aortic root dilatation rate (no losartan, 1.3+/-1.5 mm/3 years, n=59 versus losartan, 0.

20 ation rate in haploinsufficient patients (no losartan, 1.8+/-1.5 mm/3 years, n=21 versus losartan 0.5

21 ensive effects of the AT(1) receptor blocker losartan (10 mg/kg/day) were attenuated by ~15 mm Hg.

22 sive effects of cediranib were unaffected by losartan (10 mg/kg/h), bosentan (20 mg/kg/h), or a combi

23 sive effects of cediranib were unaffected by losartan (10 mg/kg/h), bosentan (20 mg/kg/h), or a combi

24 renal arterial myocytes, the AT1R antagonist losartan (10 muM) abolished the ANG-II (1 muM)-induced r

25 an patients were randomized to daily receive losartan 100 mg or no losartan.

26 dex >25 kg/m(2) to receive aliskiren 300 mg, losartan 100 mg, or their combination daily for 9 months

27 ia and who were randomly assigned to receive losartan (100 mg daily), enalapril (20 mg daily), or pla

28 e randomly assigned the patients to placebo, losartan (100 mg daily), or spironolactone (25 mg daily)

29 ndomly assigned via computer-based system to losartan (100 mg per day) or placebo for 12 months.

30 , 1.11-1.73, respectively); use of high-dose losartan (100 mg) was similar in risk (HR, 0.71; 95% CI,

31 ssigned 153 transplant recipients to receive losartan, 100 mg (n=77), or matching placebo (n=76) with

32 Among 4397 users of losartan, 1212 deaths occurred during 11,347 person-year

33 ian follow-up in each group (IQR 3.7-5.5 for losartan 150 mg; 3.4-5.5 for losartan 50 mg), 828 (43%)

34 Patients were randomly assigned between losartan (150 mg daily) and placebo with target treatmen

35 placebo group; the incidence was higher with losartan (17%, P=0.01 by the log-rank test) but not with

36 n (at a dose of 10 mg), amlodipine (2.5 mg), losartan (25 mg), and hydrochlorothiazide (12.5 mg).

37 Muscimol (80 pmol), a GABA(A) agonist, or losartan (43.4 pmol), an AT(1) receptor antagonist, atte

38 IQR 3.7-5.5 for losartan 150 mg; 3.4-5.5 for losartan 50 mg), 828 (43%) patients in the 150 mg group

39 nteers were randomly assigned to single-dose losartan (50 mg) (n = 28) versus placebo (n = 25).

40 nts were randomised to a single oral dose of losartan (50 mg) or placebo, 1 h before being exposed to

41 6-32 mg), low-dose (12.5 mg) and medium-dose losartan (50 mg) were associated with increased mortalit

42 with an angiotensin II receptor antagonist, losartan, 50 mg daily.

43 o: Nx+V receiving vehicle; Nx+L treated with losartan, 50 mg/kg/day; Nx+L+Eple, given losartan and ep

44 g the higher pharmacy costs of aliskiren and losartan ($7769), which were partially offset by savings

45 oint evaluation of Angiotensin II Antagonist Losartan), a multinational randomized trial in symptomat

46 the cognitive and cerebrovascular rescue of losartan, a commonly prescribed ARB, in a mouse model of

47 Losartan, a commonly prescribed US Food and Drug Adminis

48 We propose losartan, a drug approved by the US Food and Drug Admini

49 Losartan, a type I angiotensin II receptor (AT1R) antago

50 We tested whether losartan--a clinically approved angiotensin II receptor

51 The selective AT1 receptor blocker (ARB) losartan abrogated aneurysm progression in the mice; ful

52 Moreover, losartan activated Smad7 protein, a key negative regulat

53 s no increased mortality comparing high-dose losartan against the highest doses of candesartan.

54 s not significantly different from that with losartan alone (P=0.52).

55 antibody to all three isoforms of TGF-beta), losartan (an angiotensin receptor antagonist), or a comb

56 henotype of RenTgMK mice, and treatment with losartan [an angiotensin type 1 receptor blocker (ARB)]

57 Losartan, an angiotensin II (Ang II) receptor blocker ac

58 phy that can be attenuated by treatment with losartan, an angiotensin II (AngII) type 1 receptor bloc

59 rrent study aimed to determine the effect of losartan, an angiotensin II receptor blocker, on subpulm

60 ed ligand of the angiotensin II receptor, or losartan, an angiotensin II receptor blocker.

61 Treatment of diabetic ZDF rats with losartan, an angiotensin II receptor-1 (Agtr1) antagonis

62 Recent evidence suggests that losartan, an angiotensin II type 1 blocker that blunts T

63 l muscle remodeling following treatment with losartan, an angiotensin II type I receptor blocker.

64 Use of losartan, an angiotensin receptor type 1 blocker used wi

65 decreased muscle fibrosis and improved pain Losartan, an angiotensin-receptor blocker with anti-fibr

66 argeting the angiotensin signaling axis with losartan, an approved angiotensin system inhibitor, coul

67 Losartan, an AT1 receptor antagonist, and inhibitors of

68 nt occurred in 6 of 47 patients who received losartan and 12 of 44 who received placebo (odds ratio [

69 New users of losartan and candesartan were selected for inclusion in

70 orting data for a clinical trial on combined losartan and chemotherapy in ovarian cancer patients.

71 By life table analysis, we found that losartan and doxycycline improved the survival of Fbn1(m

72 of MMP-2 in MFS and compared the effects of losartan and doxycycline on aortic dilatation and surviv

73 ith losartan, 50 mg/kg/day; Nx+L+Eple, given losartan and eplerenone, and Nx+L+Ly, given losartan and

74 We show, in this study, that losartan and its metabolite potently inhibit monocyte re

75 Therefore, we investigated the effects of losartan and its primary metabolite on CCL2-mediated mon

76 Combining losartan and late exercise provided no additional benefi

77 losartan and eplerenone, and Nx+L+Ly, given losartan and Ly.

78 In conclusion, adding aliskiren to losartan and optimal therapy in patients with type 2 dia

79 application of the AT(1) receptor antagonist Losartan and subsequent pre-collicular transection (to r

80 of the angiotensin type 1 receptor blockers losartan and valsartan and the angiotensin-converting en

81 OSA group, all subjects continued to receive losartan and were randomly assigned to either nightly CP

82 ocyte recruitment and therefore suggest that losartan (and potentially other AT1R blocker drugs) coul

83 12 patients receiving enalapril, 6 receiving losartan, and 4 receiving placebo.

84 and 5.8 g/m(2) reductions in the aliskiren, losartan, and combination arms, respectively; P<0.0001 f

85 BP was determined in DHI, Losartan, and placebo- treated Spontaneously Hypertensiv

86 inhibitor, the angiotensin-receptor blocker losartan, and their combination on the reduction of LV m

87 Losartan (angiotensin type 1 receptor (AT1) antagonist)

88 (angiotensin-converting enzyme inhibitor) or losartan (angiotensin-receptor blocker) in FSGS mice sti

89 Young (3-month-old) mice were treated with losartan ( approximately 10 mg/kg/d, 4 months), followed

90 baseline to follow-up in the combination and losartan arms; the secondary objective was to determine

91 e conductance regulator).Objectives: To test losartan as an antiinflammatory therapy in CF using CF h

92 These were rescued by losartan at concentrations achieved by nebulization in t

93 Methods We provided losartan (at a dose of 100 mg per day) to patients with

94 s PD123319 (AT(2)R blocker), or insulin plus losartan (AT(1)R blocker, intravenously).

95 reatment with aliskiren (renin inhibitor) or losartan (AT1 antagonist) ameliorated pulmonary ECM depo

96 The blood pressure medication losartan augments fear extinction in rodents and may hav

97 and punishments to test the prediction that losartan augments learning from appetitive relative to a

98 reated in a blinded manner with atenolol- or losartan-based regimens.

99 in MFS and decrease after administration of losartan, beta-blocker therapy, or both and therefore mi

100 The AT1R antagonist losartan blocked AngII-induced, but not vasopressin-indu

101 ine model of ischemia and reperfusion (I/R), losartan blocked vascular hyperpermeability and decrease

102 ct, the removal of Tgfbr2 and treatment with losartan both delayed the progression of articular carti

103 (18)F-FPyKYNE-losartan bound with high affinity (dissociation constant

104 reased by >50% with insulin and insulin plus losartan but not with insulin plus PD123319.

105 Collectively, these results indicate that losartan can exert antimetastatic activity by inhibiting

106 ndpoints, 1D11 was equivalent or superior to losartan; coadministration of the two agents was not sup

107 patients with heart failure, overall use of losartan compared with candesartan was not associated wi

108 rmin in combination versus rosiglitazone and losartan, compared to rosiglitazone alone, after 48 week

109 glitazone and metformin or rosiglitazone and losartan confers no greater benefit than rosiglitazone a

110 The angiotensin type 1 receptor blocker losartan could fully inhibit this response.

111 cluded patients, 47 patients received 150 mg losartan daily (age, 38.0+/-12.4 years; 74% male), and 4

112 Losartan delayed disease progression, decreased right ve

113 ved vessel perfusion and drug delivery; (ii) losartan depletes matrix via inducing antifibrotic miRNA

114 Losartan did not block the antihypertrophic effects of A

115 In predefined subgroup analyses, losartan did not have a statistically significant impact

116 Furthermore, losartan did not increase cAMP in HEK 293a cells express

117 In conclusion, treatment with losartan did not lead to a statistically significant red

118 Losartan did not significantly improve RV EF in comparis

119 inopril, or angiotensin II receptor blocker, losartan, did not improve cell engraftment.

120 miR-29b levels, whereas TGF-beta blockade or losartan effectively decreased miR-29b levels in Fbn1(C1

121 entration and reduced TGF-beta1.Conclusions: Losartan effectively reversed CF- and inflammation-assoc

122 This study investigates losartan effectiveness in genetically classified subgrou

123 tment with the angiotensin type 1 antagonist losartan eliminated the difference in obstruction-induce

124 ing, both acute and 2-week administration of losartan enhanced the consolidation of extinction memory

125 This study shows that losartan enhances learning from positive relative to neg

126 rivative of the clinically used AT1R blocker losartan exhibits high binding selectivity for kidney AT

127 Compared to placebo, losartan facilitated contextual processing and enhanced

128 In contrast, in DH rats, Losartan, followed by pre-collicular and pontine transec

129 brain were also altered in mice treated with losartan for 2 weeks, in particular reduced amygdala AT1

130 ion), and G4-animals previously treated with Losartan for 30 days followed by induction of EP and con

131 mice were treated with the Tgfbr2 inhibitor losartan for 8 weeks and then euthanized for collection

132 FPyKYNE-losartan fully antagonized the Ang II pressor effect, al

133 est destruction, but animals pretreated with Losartan (G4) did not show these features.

134 ificantly between the atenolol group and the losartan group (-0.139+/-0.013 and -0.107+/-0.013 standa

135 d the enalapril group (0.005, P=0.38) or the losartan group (0.026, P=0.26), nor were there significa

136 A decrease in systolic blood pressure in the losartan group (from mean 127 mm Hg [SD 12] to 121 mm Hg

137 cular mass between the placebo group and the losartan group (mean difference 1 g/m(2), 95% CI -3 to 6

138 During the films, the losartan group recorded lower HR and higher HR variabili

139 e atenolol group and 11.0+/-6.2 years in the losartan group), who had an aortic-root z score greater

140 nd 0.29, 95% CI, 0.16-0.52; P < 0.001 in the losartan group).

141 assigned to the metoprolol group, 102 to the losartan group, and 110 to the control group.

142 In the losartan group, one (1%) patient had angioedema, one (1%

143 en group; 5.5+/-15.6/3.7+/-10.7 mm Hg in the losartan group; 6.6+/-16.6/4.6+/-10.5 mm Hg in the combi

144 as significantly lower in the metoprolol and losartan groups compared with the control group [6%, 12%

145 difference was found when the metoprolol and losartan groups were directly compared (P = 0.21).

146 Use of Losartan had dramatically beneficial effects on sarcopen

147 The local Ang II receptor (AT1R) blocker losartan had negligible effect on tone or [Ca(2+)]i in c

148 Losartan had no significant effect on RV dysfunction or

149 (18)F-FPyKYNE-losartan has a favorable binding profile and displays hi

150 Losartan has been shown to prevent aneurysms in another

151 Thus, losartan has the potential to enhance the efficacy of na

152 Losartan, HET0016, and 20-HETE antagonists each normaliz

153 armacologic inhibition using AT1R antagonist losartan, HGF and HPLF were stimulated by IL-1beta for 3

154 ment at both 2 and 9 months of age, whereas, losartan improved grip strength only at 2 months.

155 Furthermore, losartan improved the distribution and therapeutic effic

156 Through this physical mechanism, losartan improves drug and oxygen delivery to tumours, t

157 etion of IL-6 and IL-8 was not influenced by losartan in HGF or HPLF.

158 We discuss potential mechanisms of losartan in preventing PTSD symptomatology, including th

159 Aliskiren was as effective as losartan in promoting LV mass regression.

160 ing assays were performed with (18)F-FPyKYNE-losartan in rat kidneys.

161 ly attenuated the antihypertensive effect of losartan in rats with renal hypertension.

162 Aliskiren was as effective as losartan in reducing LV mass index (P<0.0001 for noninfe

163 termine whether aliskiren was noninferior to losartan in reducing LV mass index from baseline to foll

164 determine whether there might be a role for losartan in specific vulnerable subgroups.

165 al volume was lower in subjects treated with losartan in the microalbuminuria group (18.8 vs. 25.6%;

166 t angiotensin II (AngII) and inverse agonist losartan in wild-type AT1R changed the accessibility of

167 nic effects of an AT(1) receptor antagonist (losartan) in the monocrotaline PAH rat model (60 mg/kg).

168 cells that express endogenous AT1R and D1R, losartan increased cAMP generation.

169 Losartan increased cAMP in HEK 293a cells transfected wi

170 We found that adding aliskiren to losartan increased time free of ESRD, life expectancy, a

171 with either receptor alone, suggesting that losartan induces D1R activation.

172 AP on the cardiovascular effects of chronic losartan infusion in order to test the hypothesis that a

173 We found that losartan inhibited collagen I production by carcinoma-as

174 Administration of losartan inhibited TGF-beta signaling pathway, resulting

175 ]-AngII, but not the neutral AT1 antagonist, losartan, inhibits endogenous B2 receptor signaling.

176 A prophylactic treatment with metoprolol or losartan, initiated soon after lung cancer surgery in pa

177 er prophylactic treatment with metoprolol or losartan, initiated soon after lung cancer surgery in pa

178 409 hypertensive patients in the LIFE study (Losartan Intervention For End-point reduction in hyperte

179 In the Losartan Intervention for Endpoint Reduction (LIFE) echo

180 Injections of losartan into the LV blocked the dipsogenic response to

181 The angiotensin-II antagonist losartan is a promising candidate that has enhanced exti

182 nctional and physiological outcomes and that losartan is a viable candidate for translational studies

183 Chronic inhibition of RAAS by losartan is beneficial in experimental PAH.

184 Losartan is exceptional amongst antihypertensive drugs i

185 mediated platelet aggregation as compared to losartan (LOS) (collagen, IC50 = 10.4 muM; CRP-XL, IC50

186 evaluate the effect of Telmisartan (Tel) and Losartan (Los) on nanoparticle intratumoral distribution

187 neal injections of TNF (30 microg/kg), TNF + losartan (LOS, 1 mg/kg), or vehicle for 5 days.

188 As an add-on to losartan, Ly normalized blood pressure and albuminuria,

189 ults from observational studies suggest that losartan may be associated with increased mortality in p

190 h regard to slowing aortic-root enlargement, losartan may be more effective than beta-blockers, the c

191 These data suggest that losartan may be used for blocking vascular hyperpermeabi

192 knockdown and AT1R pharmacologic blockade by losartan may differently control balance of inflammatory

193 Treatment with losartan may preserve some features of kidney structure

194 Mechanistically, losartan-mediated inhibition of vascular hyperpermeabili

195 i-inflammatory effects, but failed to modify losartan-mediated reductions in oxidative stress.

196 %), and central antagonism of AT1 receptors (losartan) microinjected into the lateral ventricle reduc

197 Taken together, these data imply that losartan might exert its antihypertensive effect both by

198 Pharmacologic inhibition of AT1R through losartan modulated mRNA transcription of IL-6 and IL-8 i

199 s not significantly different from that with losartan monotherapy, independent of blood pressure lowe

200 MFS patients treated with losartan (n=55) or beta-blocker (n=80) showed significan

201 were randomly assigned to placebo (n=69) or losartan (n=64).

202 In contrast, neither losartan nor chelerythrine had any effect on mEPSCs or p

203 Neither losartan nor divalinal affected arterial blood pressure

204 d blockade of the ANGII receptor type 1 with losartan normalizes BP.

205 interval [CI], 0.14 to 0.85) and by 70% with losartan (odds ratio, 0.30; 95% CI, 0.12 to 0.73), indep

206 red the effects of high-dose versus low-dose losartan on clinical outcomes in patients with heart fai

207 erlying these results, testing the effect of losartan on data-driven and contextual processing of tra

208 ffect of the angiotensin II receptor blocker losartan on left ventricular hypertrophy and fibrosis in

209 ever, the role of MMP-2 in MFS and effect of losartan on the lifespan of MFS mice remain unknown.

210 We found no significant effect of losartan on time to a composite of ESRD, death, or doubl

211 the effect of the AngII receptor antagonist, losartan, on the drinking response to AngII injected int

212 mg of rosiglitazone twice-daily and 50 mg of losartan once-daily for 48 weeks.

213 placental apoptosis are diminished by either losartan or an autoantibody-neutralizing peptide.

214 fan's syndrome who were randomly assigned to losartan or atenolol, we found no significant difference

215 In addition, microinjection of losartan or chelerythrine into the PVN substantially red

216 ere we show that blocking AT1 receptors with losartan or inhibiting PKC with chelerythrine significan

217 Subjects received 100 mg losartan or placebo daily.

218 ) /dy(2J) and control mice were treated with losartan or placebo for 12 weeks from 6 weeks of age.

219 th this hypothesis, antagonism of AT1R using losartan or shRNA-mediated knockdown in melanoma cell li

220 locked by an antagonist of AngII receptor I, losartan, or overexpression of single mutant S303A of IR

221 ne were randomized to a mean of 4.8 years of losartan- or atenolol-based treatment.

222 line electrocardiogram, randomly assigned to losartan- or atenolol-based treatment.

223 ed with renin-angiotensin system inhibition (losartan plus enalapril).

224 In contrast, losartan plus insulin increased muscle MBV by two- to th

225 tments with either isoflurane anaesthesia or losartan prevented early microvascular damage and late e

226 etes, but treatment with either captopril or losartan prevented these effects.

227 Most importantly, losartan prevents the development of delayed recurrent s

228 e angiotensin II type 1 receptor antagonist, losartan, previously identified as a blocker of peripher

229 nt a novel combinatorial treatment utilizing losartan, previously shown to ameliorate fibrosis and in

230 Losartan protects against myocardial ischemia and reperf

231 Losartan reduced BP in OSA, but the reductions were less

232 Treatment with losartan reduced left ventricular dysfunction and preven

233 However, losartan reduced only aortic root dilatation rate in hap

234 It has been shown that losartan reduces aortic dilatation in patients with Marf

235 Consequently, losartan reduces solid stress in tumours resulting in in

236 e demonstrate that the angiotensin inhibitor losartan reduces stromal collagen and hyaluronan product

237 in NIDDM with the Angiotensin II Antagonist Losartan (RENAAL) trial with independent replication in

238 Nebulized losartan rescued both mucus transport and mucus hypercon

239 The mechanism depicting how ARBs such as losartan restore cerebrovascular and cognitive deficits

240 Divalinal reverted losartan's anti-inflammatory effects, but failed to modi

241 ine model of CF-like airway disease.Methods: Losartan's antiinflammatory effectiveness to rescue BK a

242 /AT4R cascade as the underlying mechanism in losartan's benefits and a target that could restore Abet

243 Here, we propose a mechanism underlying losartan's benefits by selectively blocking the effects

244 scue spatial learning and memory and blocked losartan's benefits on dilatory function and baseline ni

245 Divalinal countered losartan's capacity to rescue spatial learning and memor

246 Losartan's effects on transforming growth factor beta (T

247 In a secondary analysis, losartan seemed to reduce the risk of a composite of dou

248 Finally, the prototypic AT(1)R antagonist losartan seems unable to lower this adrenal betaarr1-dri

249 e to the angiotensin receptor type 1 blocker losartan showed decreased JNK phosphorylation.

250 Overall, losartan significantly reduced aortic root dilatation ra

251 Losartan significantly reduced learning rates from avers

252 Losartan significantly reduced systolic, diastolic, and

253 In this study, the AT1R antagonist losartan strengthened the interaction between AT1R and D

254 the AngII type 1 receptor (AT1R) antagonist, losartan, suggesting that the observed effect was mediat

255 ct on PTSD may be driven more by ARBs (e.g., Losartan) than by ACE-Is.

256 njected into 4V, even when we used a dose of losartan that was 25 times greater than needed when inje

257 he angiotensin II type 1 receptor antagonist losartan, the oxytocin receptor antagonist desGly-NH2 ,

258 r resistance to chemotherapy; (iii) although losartan therapy alone does not reduce tumor burden, it

259 FBN1 mutations seem to be more responsive to losartan therapy for inhibition of aortic root dilatatio

260 Application of losartan to inhibit collagen binding to GPVI resulted in

261 e anti-fibrotic angiotensin receptor blocker losartan to mice in drinking water reduced both allodyni

262 he angiotensin II type 1 receptor antagonist losartan to mutation-positive, hypertrophy-negative (pre

263 ion, the addition of spironolactone, but not losartan, to a regimen including maximal ACE inhibition

264 P; G2-animals with EP treated with water; G3-Losartan-treated animals (treatment started at the same

265 Losartan-treated Fbn1(C1039G/+) mice had lower total TGF

266 oved cardiac structure and function, whereas losartan-treated mice had no improvement.

267 This study hypothesized that Losartan treatment could promote protection to rats subm

268 Losartan treatment did not reverse pathologic remodeling

269 report here four translatable findings: (i) losartan treatment enhances the efficacy of paclitaxel-a

270 Inhibition of TGFbeta signaling by Losartan treatment greatly improved the phenotype of myo

271 s study support pursuing a clinical trial of losartan treatment in children with MDC1A.

272 We therefore evaluated the effect of losartan treatment in the dy(2J) /dy(2J) mouse model of

273 In addition, losartan treatment inhibited the MAPK cascade as shown b

274 rimental metastasis models demonstrated that losartan treatment significantly reduced the metastatic

275 Losartan treatment was associated with significant impre

276 After losartan treatment, we performed classical Pavlovian fea

277 Losartan treatment, which lowers TGFbeta signaling and r

278 sing Morris water mazes at 3 and 4 months of losartan treatment.

279 However, Losartan treatments attenuated these responses in additi

280 r-beta (TGFbeta) signaling in the aorta, but losartan uniquely inhibited TGFbeta-mediated activation

281 s was affected for generic versus brand-name losartan users only (difference of proportions, 2.0% [0.

282 Rates of adverse events for losartan, valsartan, and candesartan users (N=136 177) a

283 Among generic users of losartan, valsartan, and candesartan, there was an incre

284 e 2 diabetes enrolled in a clinical trial of losartan versus placebo.

285 FR outcome, and the unadjusted hazard ratio (losartan vs. placebo) was 0.50 (95% CI, 0.12-1.99).

286 FS mutant mice (Fbn1(C1039G/+)) treated with losartan was analyzed for circulating TGF-beta1 concentr

287 However, in a post hoc analysis, losartan was associated with improved RV EF in a subgrou

288 The angiotensin receptor blocker losartan was given to half the animals.

289 There was no effect, however, when losartan was injected into 4V, even when we used a dose

290 Compared with candesartan, losartan was not associated with increased all-cause mor

291 mass with the combination of aliskiren plus losartan was not significantly different from that with

292 Treatment with losartan was safe, suggesting that it can be used for ot

293 angiotensin receptor type 1 (AT1) antagonist losartan, we investigated the acute and long-term effect

294 Although low doses of losartan were associated with increased mortality, there

295 d heart rate responses to 10-day infusion of losartan were compared in sham rats and those with dual

296 Conversely, irbesartan and losartan were largely G protein-selective inhibitors at

297 retreated with the conventional AT1R blocker losartan were unable to enhance cardiac contractility wi

298 Administration of losartan, which blocks all type 1 angiotensin receptors,

299 We conducted a randomized trial comparing losartan with atenolol in children and young adults with

300 er attenuation of the hypotensive effects of losartan would be observed in rats with dual lesions.