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1  the Ang II type 1 (AT1) receptor antagonist losartan.
2 levels and these effects were not blocked by losartan.
3 ment with the Ang II type 1 receptor blocker losartan.
4 ith the addition of either spironolactone or losartan.
5 , +10.5%, P = 0.20) in the group assigned to losartan.
6 ime costs for aliskiren plus losartan versus losartan.
7 II accumulation induced by hyperglycemia and losartan.
8 angiotensin II in the absence or presence of losartan.
9    The crossover also included amiloride and losartan.
10  chronic intracerebroventricular delivery of losartan.
11 ntions were used; isoflurane anaesthesia and losartan.
12 as managed with prednisone, alendronate, and losartan.
13 ial that assessed renoprotective efficacy of losartan.
14  pressor response of 25.5 mg/kg) relative to losartan.
15 mized to daily receive losartan 100 mg or no losartan.
16 he angiotensin II type 1 receptor antagonist losartan.
17  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
18  losartan, 1.2+/-1.7 mm/3 years, n=38 versus losartan 0.8+/-1.3 mm/3 years, n=41; P=0.197).
19  losartan, 1.3+/-1.5 mm/3 years, n=59 versus losartan, 0.8+/-1.4 mm/3 years, n=58; P=0.009).
20  versus Ang II); adding the AT(1) antagonist losartan (1 microm) resulted in Ang II stimulating NO by
21                   Further, the AT1 R blocker losartan (1 mum) diminished myogenic tone and blocked st
22                      Dose-ranging studies of losartan (1-50 mg/kg) were initially conducted in a rat
23    Captopril alone (1.78 +/- 0.31%) and with losartan (1.13 +/- 0.28%) significantly reduced tracer u
24 ment with an Ang II type 1 receptor blocker (losartan, 1 micromol/l), calcineurin inhibitor (cyclospo
25 1) and not in dominant negative patients (no losartan, 1.2+/-1.7 mm/3 years, n=38 versus losartan 0.8
26 ntly reduced aortic root dilatation rate (no losartan, 1.3+/-1.5 mm/3 years, n=59 versus losartan, 0.
27 ation rate in haploinsufficient patients (no losartan, 1.8+/-1.5 mm/3 years, n=21 versus losartan 0.5
28 ensive effects of the AT(1) receptor blocker losartan (10 mg/kg/day) were attenuated by ~15 mm Hg.
29 sive effects of cediranib were unaffected by losartan (10 mg/kg/h), bosentan (20 mg/kg/h), or a combi
30 sive effects of cediranib were unaffected by losartan (10 mg/kg/h), bosentan (20 mg/kg/h), or a combi
31 renal arterial myocytes, the AT1R antagonist losartan (10 muM) abolished the ANG-II (1 muM)-induced r
32                                              Losartan (10(-10) to 10(-6)M) was further tested ex vivo
33 an patients were randomized to daily receive losartan 100 mg or no losartan.
34 dex >25 kg/m(2) to receive aliskiren 300 mg, losartan 100 mg, or their combination daily for 9 months
35 ia and who were randomly assigned to receive losartan (100 mg daily), enalapril (20 mg daily), or pla
36 e randomly assigned the patients to placebo, losartan (100 mg daily), or spironolactone (25 mg daily)
37 ndomly assigned via computer-based system to losartan (100 mg per day) or placebo for 12 months.
38 , 1.11-1.73, respectively); use of high-dose losartan (100 mg) was similar in risk (HR, 0.71; 95% CI,
39 ssigned 153 transplant recipients to receive losartan, 100 mg (n=77), or matching placebo (n=76) with
40 abetic nephropathy, addition of aliskiren to losartan, 100 mg resulted in a 20% greater reduction in
41                          Among 4397 users of losartan, 1212 deaths occurred during 11,347 person-year
42 e (ACE) inhibitors were randomly assigned to losartan 150 mg (n=1927) or 50 mg daily (n=1919).
43                                              Losartan 150 mg daily reduced the rate of death or admis
44 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%)
45      Patients were randomly assigned between losartan (150 mg daily) and placebo with target treatmen
46 placebo group; the incidence was higher with losartan (17%, P=0.01 by the log-rank test) but not with
47                  The AT1 receptor antagonist losartan (2 microm, n = 6) abolished all responses to An
48    Muscimol (80 pmol), a GABA(A) agonist, or losartan (43.4 pmol), an AT(1) receptor antagonist, atte
49  intolerance to ACE inhibitors compared with losartan 50 mg daily.
50 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
51 6-32 mg), low-dose (12.5 mg) and medium-dose losartan (50 mg) were associated with increased mortalit
52  with an angiotensin II receptor antagonist, losartan, 50 mg daily.
53 o: Nx+V receiving vehicle; Nx+L treated with losartan, 50 mg/kg/day; Nx+L+Eple, given losartan and ep
54 g the higher pharmacy costs of aliskiren and losartan ($7769), which were partially offset by savings
55 oint evaluation of Angiotensin II Antagonist Losartan), a multinational randomized trial in symptomat
56  the cognitive and cerebrovascular rescue of losartan, a commonly prescribed ARB, in a mouse model of
57                                              Losartan, a commonly prescribed US Food and Drug Adminis
58                                   We propose losartan, a drug approved by the US Food and Drug Admini
59                            We tested whether losartan--a clinically approved angiotensin II receptor
60     The selective AT1 receptor blocker (ARB) losartan abrogated aneurysm progression in the mice; ful
61                                    Moreover, losartan activated Smad7 protein, a key negative regulat
62 s no increased mortality comparing high-dose losartan against the highest doses of candesartan.
63 s not significantly different from that with losartan alone (P=0.52).
64                  Treatment with enalapril or losartan also decreased renal plasminogen activator inhi
65                                              Losartan also suppressed tumor necrosis factor alpha gen
66 antibody to all three isoforms of TGF-beta), losartan (an angiotensin receptor antagonist), or a comb
67 vealed it to be insensitive to inhibition by losartan (an AT(1) receptor antagonist) and PD123319 (an
68 is, which was abrogated by co-treatment with losartan (an AT-1R antagonist), wortmannin (a phosphoino
69 henotype of RenTgMK mice, and treatment with losartan [an angiotensin type 1 receptor blocker (ARB)]
70 phy that can be attenuated by treatment with losartan, an angiotensin II (AngII) type 1 receptor bloc
71 rrent study aimed to determine the effect of losartan, an angiotensin II receptor blocker, on subpulm
72 ed ligand of the angiotensin II receptor, or losartan, an angiotensin II receptor blocker.
73          Treatment of diabetic ZDF rats with losartan, an angiotensin II receptor-1 (Agtr1) antagonis
74                Recent evidence suggests that losartan, an angiotensin II type 1 blocker that blunts T
75 l muscle remodeling following treatment with losartan, an angiotensin II type I receptor blocker.
76  angiotensin-converting enzyme inhibitors or losartan, an angiotensin receptor blocker, will decrease
77                                       Use of losartan, an angiotensin receptor type 1 blocker used wi
78 features were prevented by co-injection with losartan, an AT(1) receptor antagonist, or by an antibod
79                                              Losartan, an AT1 receptor antagonist, and inhibitors of
80 nt occurred in 6 of 47 patients who received losartan and 12 of 44 who received placebo (odds ratio [
81                                 New users of losartan and candesartan were selected for inclusion in
82        By life table analysis, we found that losartan and doxycycline improved the survival of Fbn1(m
83  of MMP-2 in MFS and compared the effects of losartan and doxycycline on aortic dilatation and surviv
84 ith losartan, 50 mg/kg/day; Nx+L+Eple, given losartan and eplerenone, and Nx+L+Ly, given losartan and
85 s were diminished in animals pretreated with losartan and in those deficient for the ATII receptor 1a
86  losartan and eplerenone, and Nx+L+Ly, given losartan and Ly.
87 f 300 mg/d to the highest approved dosage of losartan and optimal antihypertensive therapy reduces al
88           In conclusion, adding aliskiren to losartan and optimal therapy in patients with type 2 dia
89 ney injury; however, combined treatment with losartan and paricalcitol completely prevented albuminur
90 application of the AT(1) receptor antagonist Losartan and subsequent pre-collicular transection (to r
91 otensin-II (A-II) type 1 receptor antagonist losartan and the nonspecific A-II receptor antagonist sa
92 ere inhibited by the AT1 receptor antagonist losartan and the phospholipase C (PLC) inhibitor U73122.
93  of the angiotensin type 1 receptor blockers losartan and valsartan and the angiotensin-converting en
94 OSA group, all subjects continued to receive losartan and were randomly assigned to either nightly CP
95 12 patients receiving enalapril, 6 receiving losartan, and 4 receiving placebo.
96 y the angiotensin II type 1 receptor blocker losartan, and by the NADPH oxidase inhibitor apocynin.
97  and 5.8 g/m(2) reductions in the aliskiren, losartan, and combination arms, respectively; P<0.0001 f
98                    BP was determined in DHI, Losartan, and placebo- treated Spontaneously Hypertensiv
99  inhibitor, the angiotensin-receptor blocker losartan, and their combination on the reduction of LV m
100                                              Losartan (angiotensin type 1 receptor (AT1) antagonist)
101 (angiotensin-converting enzyme inhibitor) or losartan (angiotensin-receptor blocker) in FSGS mice sti
102   Young (3-month-old) mice were treated with losartan ( approximately 10 mg/kg/d, 4 months), followed
103 baseline to follow-up in the combination and losartan arms; the secondary objective was to determine
104 red smooth muscle cells (SMC) was reduced by losartan, as was SMC invasion through an elastin gel bar
105                          Methods We provided losartan (at a dose of 100 mg per day) to patients with
106 s PD123319 (AT(2)R blocker), or insulin plus losartan (AT(1)R blocker, intravenously).
107 reatment with aliskiren (renin inhibitor) or losartan (AT1 antagonist) ameliorated pulmonary ECM depo
108 reated in a blinded manner with atenolol- or losartan-based regimens.
109  in MFS and decrease after administration of losartan, beta-blocker therapy, or both and therefore mi
110                          The AT1R antagonist losartan blocked AngII-induced, but not vasopressin-indu
111 ct, the removal of Tgfbr2 and treatment with losartan both delayed the progression of articular carti
112                                (18)F-FPyKYNE-losartan bound with high affinity (dissociation constant
113 was blocked by the selective AT1R antagonist losartan but not by the selective AT2R antagonist PD1233
114 reased by >50% with insulin and insulin plus losartan but not with insulin plus PD123319.
115 an angiotensin II (AT)1 receptor antagonist (losartan), but not by an AT2 receptor blocker (PD123319)
116 ndpoints, 1D11 was equivalent or superior to losartan; coadministration of the two agents was not sup
117 rated a significantly attenuated response to losartan compared to sham animals but showed no greater
118  patients with heart failure, overall use of losartan compared with candesartan was not associated wi
119 rmin in combination versus rosiglitazone and losartan, compared to rosiglitazone alone, after 48 week
120 glitazone and metformin or rosiglitazone and losartan confers no greater benefit than rosiglitazone a
121                    Next, we examined whether losartan could improve impaired responses of cerebral ar
122 cluded patients, 47 patients received 150 mg losartan daily (age, 38.0+/-12.4 years; 74% male), and 4
123 roduction in nondiabetics and diabetics, and losartan decreased basal (diabetics) and angiotensin II-
124 gnaling, with the ATII receptor 1a inhibitor losartan, decreased LPS-induced pulmonary neutrophil rec
125                                              Losartan delayed disease progression, decreased right ve
126                           In addition, while losartan did not alter responses in nondiabetics, losart
127                                              Losartan did not block the antihypertrophic effects of A
128             In predefined subgroup analyses, losartan did not have a statistically significant impact
129                                 Furthermore, losartan did not increase cAMP in HEK 293a cells express
130                In conclusion, treatment with losartan did not lead to a statistically significant red
131                                              Losartan did not significantly improve RV EF in comparis
132 inopril, or angiotensin II receptor blocker, losartan, did not improve cell engraftment.
133                                Enalapril and losartan each reduced hypertension, proteinuria, glomeru
134 miR-29b levels, whereas TGF-beta blockade or losartan effectively decreased miR-29b levels in Fbn1(C1
135                      This study investigates losartan effectiveness in genetically classified subgrou
136 tment with the angiotensin type 1 antagonist losartan eliminated the difference in obstruction-induce
137 ing, both acute and 2-week administration of losartan enhanced the consolidation of extinction memory
138 rivative of the clinically used AT1R blocker losartan exhibits high binding selectivity for kidney AT
139                     In contrast, in DH rats, Losartan, followed by pre-collicular and pontine transec
140  mice were treated with the AngII antagonist losartan for 12 wk.
141 brain were also altered in mice treated with losartan for 2 weeks, in particular reduced amygdala AT1
142  mice were treated with the Tgfbr2 inhibitor losartan for 8 weeks and then euthanized for collection
143                                      FPyKYNE-losartan fully antagonized the Ang II pressor effect, al
144 ificantly between the atenolol group and the losartan group (-0.139+/-0.013 and -0.107+/-0.013 standa
145 d the enalapril group (0.005, P=0.38) or the losartan group (0.026, P=0.26), nor were there significa
146 A decrease in systolic blood pressure in the losartan group (from mean 127 mm Hg [SD 12] to 121 mm Hg
147 cular mass between the placebo group and the losartan group (mean difference 1 g/m(2), 95% CI -3 to 6
148 e atenolol group and 11.0+/-6.2 years in the losartan group), who had an aortic-root z score greater
149 nd 0.29, 95% CI, 0.16-0.52; P < 0.001 in the losartan group).
150 assigned to the metoprolol group, 102 to the losartan group, and 110 to the control group.
151                                       In the losartan group, one (1%) patient had angioedema, one (1%
152 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
153 as significantly lower in the metoprolol and losartan groups compared with the control group [6%, 12%
154 difference was found when the metoprolol and losartan groups were directly compared (P = 0.21).
155                                       Use of Losartan had dramatically beneficial effects on sarcopen
156     The local Ang II receptor (AT1R) blocker losartan had negligible effect on tone or [Ca(2+)]i in c
157                                              Losartan had no significant effect on RV dysfunction or
158                                (18)F-FPyKYNE-losartan has a favorable binding profile and displays hi
159                                              Losartan has been shown to prevent aneurysms in another
160                                        Thus, losartan has the potential to enhance the efficacy of na
161                                              Losartan, HET0016, and 20-HETE antagonists each normaliz
162 armacologic inhibition using AT1R antagonist losartan, HGF and HPLF were stimulated by IL-1beta for 3
163 ment at both 2 and 9 months of age, whereas, losartan improved grip strength only at 2 months.
164                                 Furthermore, losartan improved the distribution and therapeutic effic
165             Through this physical mechanism, losartan improves drug and oxygen delivery to tumours, t
166                                  The ARB was losartan in 17 patients and irbesartan in 1 patient.
167 etion of IL-6 and IL-8 was not influenced by losartan in HGF or HPLF.
168                Aliskiren was as effective as losartan in promoting LV mass regression.
169 ing assays were performed with (18)F-FPyKYNE-losartan in rat kidneys.
170 ly attenuated the antihypertensive effect of losartan in rats with renal hypertension.
171                Aliskiren was as effective as losartan in reducing LV mass index (P<0.0001 for noninfe
172 termine whether aliskiren was noninferior to losartan in reducing LV mass index from baseline to foll
173  determine whether there might be a role for losartan in specific vulnerable subgroups.
174 al volume was lower in subjects treated with losartan in the microalbuminuria group (18.8 vs. 25.6%;
175 t angiotensin II (AngII) and inverse agonist losartan in wild-type AT1R changed the accessibility of
176 nic effects of an AT(1) receptor antagonist (losartan) in the monocrotaline PAH rat model (60 mg/kg).
177 d an angiotensin II type 1 receptor blocker (losartan) in thymic stromal lymphopoietin transgenic (TS
178  cells that express endogenous AT1R and D1R, losartan increased cAMP generation.
179                                              Losartan increased cAMP in HEK 293a cells transfected wi
180            We found that adding aliskiren to losartan increased time free of ESRD, life expectancy, a
181  with either receptor alone, suggesting that losartan induces D1R activation.
182  AP on the cardiovascular effects of chronic losartan infusion in order to test the hypothesis that a
183                                              Losartan inhibited acute joint inflammation in a dose-de
184                                We found that losartan inhibited collagen I production by carcinoma-as
185                            Administration of losartan inhibited TGF-beta signaling pathway, resulting
186 ]-AngII, but not the neutral AT1 antagonist, losartan, inhibits endogenous B2 receptor signaling.
187 er prophylactic treatment with metoprolol or losartan, initiated soon after lung cancer surgery in pa
188  A prophylactic treatment with metoprolol or losartan, initiated soon after lung cancer surgery in pa
189 409 hypertensive patients in the LIFE study (Losartan Intervention For End-point reduction in hyperte
190                                       In the Losartan Intervention for Endpoint Reduction (LIFE) echo
191 eline electrocardiogram, and enrolled in the Losartan Intervention for Endpoint Reduction in Hyperten
192                                Injections of losartan into the LV blocked the dipsogenic response to
193                Chronic inhibition of RAAS by losartan is beneficial in experimental PAH.
194                                              Losartan is exceptional amongst antihypertensive drugs i
195 mediated platelet aggregation as compared to losartan (LOS) (collagen, IC50 = 10.4 muM; CRP-XL, IC50
196 evaluate the effect of Telmisartan (Tel) and Losartan (Los) on nanoparticle intratumoral distribution
197 neal injections of TNF (30 microg/kg), TNF + losartan (LOS, 1 mg/kg), or vehicle for 5 days.
198                              As an add-on to losartan, Ly normalized blood pressure and albuminuria,
199 ults from observational studies suggest that losartan may be associated with increased mortality in p
200 h regard to slowing aortic-root enlargement, losartan may be more effective than beta-blockers, the c
201 knockdown and AT1R pharmacologic blockade by losartan may differently control balance of inflammatory
202                               Treatment with losartan may preserve some features of kidney structure
203 i-inflammatory effects, but failed to modify losartan-mediated reductions in oxidative stress.
204    Inhibition by an AT1 receptor antagonist (losartan metabolite: E3174) or catalase, confirmed that
205 %), and central antagonism of AT1 receptors (losartan) microinjected into the lateral ventricle reduc
206        Taken together, these data imply that losartan might exert its antihypertensive effect both by
207     Pharmacologic inhibition of AT1R through losartan modulated mRNA transcription of IL-6 and IL-8 i
208 s not significantly different from that with losartan monotherapy, independent of blood pressure lowe
209                    MFS patients treated with losartan (n=55) or beta-blocker (n=80) showed significan
210  were randomly assigned to placebo (n=69) or losartan (n=64).
211                                      Neither losartan nor divalinal affected arterial blood pressure
212 d blockade of the ANGII receptor type 1 with losartan normalizes BP.
213 r the angiotensin II type 1 receptor blocker losartan normalizes muscle architecture, repair and func
214 interval [CI], 0.14 to 0.85) and by 70% with losartan (odds ratio, 0.30; 95% CI, 0.12 to 0.73), indep
215 red the effects of high-dose versus low-dose losartan on clinical outcomes in patients with heart fai
216 ffect of the angiotensin II receptor blocker losartan on left ventricular hypertrophy and fibrosis in
217 ever, the role of MMP-2 in MFS and effect of losartan on the lifespan of MFS mice remain unknown.
218            We found no significant effect of losartan on time to a composite of ESRD, death, or doubl
219 the effect of the AngII receptor antagonist, losartan, on the drinking response to AngII injected int
220 mg of rosiglitazone twice-daily and 50 mg of losartan once-daily for 48 weeks.
221 ty, which was abolished by co-treatment with losartan or 2',5'-dideoxyadenosine (2',5'-DOA, an adenyl
222 placental apoptosis are diminished by either losartan or an autoantibody-neutralizing peptide.
223 fan's syndrome who were randomly assigned to losartan or atenolol, we found no significant difference
224          Treatment of the diabetic mice with losartan or paricalcitol (19-nor-1,25-dihydroxyvitamin D
225                     Subjects received 100 mg losartan or placebo daily.
226 ) /dy(2J) and control mice were treated with losartan or placebo for 12 weeks from 6 weeks of age.
227 locked by an antagonist of AngII receptor I, losartan, or overexpression of single mutant S303A of IR
228 ne were randomized to a mean of 4.8 years of losartan- or atenolol-based treatment.
229 line electrocardiogram, randomly assigned to losartan- or atenolol-based treatment.
230 ed with renin-angiotensin system inhibition (losartan plus enalapril).
231                                 In contrast, losartan plus insulin increased muscle MBV by two- to th
232 tments with either isoflurane anaesthesia or losartan prevented early microvascular damage and late e
233 etes, but treatment with either captopril or losartan prevented these effects.
234                            Most importantly, losartan prevents the development of delayed recurrent s
235 e angiotensin II type 1 receptor antagonist, losartan, previously identified as a blocker of peripher
236 nt a novel combinatorial treatment utilizing losartan, previously shown to ameliorate fibrosis and in
237                                              Losartan reduced BP in OSA, but the reductions were less
238                               Treatment with losartan reduced left ventricular dysfunction and preven
239                                     However, losartan reduced only aortic root dilatation rate in hap
240                       It has been shown that losartan reduces aortic dilatation in patients with Marf
241                                Consequently, losartan reduces solid stress in tumours resulting in in
242 e demonstrate that the angiotensin inhibitor losartan reduces stromal collagen and hyaluronan product
243  in NIDDM with the Angiotensin II Antagonist Losartan (RENAAL) trial with independent replication in
244     The mechanism depicting how ARBs such as losartan restore cerebrovascular and cognitive deficits
245 tan did not alter responses in nondiabetics, losartan restored impaired eNOS-dependent vasodilatation
246                           Divalinal reverted losartan's anti-inflammatory effects, but failed to modi
247 /AT4R cascade as the underlying mechanism in losartan's benefits and a target that could restore Abet
248      Here, we propose a mechanism underlying losartan's benefits by selectively blocking the effects
249 scue spatial learning and memory and blocked losartan's benefits on dilatory function and baseline ni
250                          Divalinal countered losartan's capacity to rescue spatial learning and memor
251 animals but showed no greater attenuation of losartan's chronic hypotensive effects than animals with
252                                              Losartan's effects on transforming growth factor beta (T
253                     In a secondary analysis, losartan seemed to reduce the risk of a composite of dou
254    Finally, the prototypic AT(1)R antagonist losartan seems unable to lower this adrenal betaarr1-dri
255 e to the angiotensin receptor type 1 blocker losartan showed decreased JNK phosphorylation.
256                                     Overall, losartan significantly reduced aortic root dilatation ra
257                                              Losartan significantly reduced systolic, diastolic, and
258           In this study, the AT1R antagonist losartan strengthened the interaction between AT1R and D
259 nd therapeutic administration of 15 mg/kg of losartan substantially reduced knee joint swelling in ra
260 njected into 4V, even when we used a dose of losartan that was 25 times greater than needed when inje
261 he angiotensin II type 1 receptor antagonist losartan, the oxytocin receptor antagonist desGly-NH2 ,
262 FBN1 mutations seem to be more responsive to losartan therapy for inhibition of aortic root dilatatio
263 he angiotensin II type 1 receptor antagonist losartan to mutation-positive, hypertrophy-negative (pre
264 ion, the addition of spironolactone, but not losartan, to a regimen including maximal ACE inhibition
265                                              Losartan-treated Fbn1(C1039G/+) mice had lower total TGF
266 oved cardiac structure and function, whereas losartan-treated mice had no improvement.
267                      Overall, enalapril- and losartan-treated TSLPtg mice survived significantly long
268                                              Losartan treatment did not reverse pathologic remodeling
269           Inhibition of TGFbeta signaling by Losartan treatment greatly improved the phenotype of myo
270 s study support pursuing a clinical trial of losartan treatment in children with MDC1A.
271         We therefore evaluated the effect of losartan treatment in the dy(2J) /dy(2J) mouse model of
272                                 In addition, losartan treatment inhibited the MAPK cascade as shown b
273                                              Losartan treatment was associated with significant impre
274                                        After losartan treatment, we performed classical Pavlovian fea
275                                              Losartan treatment, which lowers TGFbeta signaling and r
276 sing Morris water mazes at 3 and 4 months of losartan treatment.
277 r-beta (TGFbeta) signaling in the aorta, but losartan uniquely inhibited TGFbeta-mediated activation
278 vely; 8 received captopril or captopril with losartan up to 4 weeks after MI.
279 s was affected for generic versus brand-name losartan users only (difference of proportions, 2.0% [0.
280                  Rates of adverse events for losartan, valsartan, and candesartan users (N=136 177) a
281                       Among generic users of losartan, valsartan, and candesartan, there was an incre
282 years, and lifetime costs for aliskiren plus losartan versus losartan.
283 FR outcome, and the unadjusted hazard ratio (losartan vs. placebo) was 0.50 (95% CI, 0.12-1.99).
284 FS mutant mice (Fbn1(C1039G/+)) treated with losartan was analyzed for circulating TGF-beta1 concentr
285             However, in a post hoc analysis, losartan was associated with improved RV EF in a subgrou
286             The angiotensin receptor blocker losartan was given to half the animals.
287           There was no effect, however, when losartan was injected into 4V, even when we used a dose
288                   Compared with candesartan, losartan was not associated with increased all-cause mor
289  mass with the combination of aliskiren plus losartan was not significantly different from that with
290                               Treatment with losartan was safe, suggesting that it can be used for ot
291 angiotensin receptor type 1 (AT1) antagonist losartan, we investigated the acute and long-term effect
292                        Although low doses of losartan were associated with increased mortality, there
293 d heart rate responses to 10-day infusion of losartan were compared in sham rats and those with dual
294                   Conversely, irbesartan and losartan were largely G protein-selective inhibitors at
295 retreated with the conventional AT1R blocker losartan were unable to enhance cardiac contractility wi
296                            Administration of losartan, which blocks all type 1 angiotensin receptors,
297 l of the selective AT(1) receptor antagonist losartan, which is currently used for the treatment of c
298    We conducted a randomized trial comparing losartan with atenolol in children and young adults with
299 ombining angiotensin II receptor blockade by losartan with beta-blocker treatment is an effective tre
300 er attenuation of the hypotensive effects of losartan would be observed in rats with dual lesions.

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