ライフサイエンスコーパス: AT1 receptor

1 AT1 receptor blockade (candesartan) and ACE inhibition (

2 AT1 receptor expression was increased (62%) and AT2 expr

3 AT1 receptors in the hypothalamus are endogenously activ

4 AT1 receptors in the NTS can depress the baroreceptor re

5 AT1 receptors were more abundant than AT2 receptors in t

6 trolyte balances, the angiotensin II type 1 (AT1) receptor activates mitogen-activated protein kinase

7 RNA and protein expression of Ang II type 1 (AT1) receptor and subunits of NAD(P)H oxidase (p40phox,

8 te ACE inhibition and angiotensin II type 1 (AT1) receptor antagonism have similar effects in patient

9 ravenous injection of angiotensin II type 1 (AT1) receptor antagonist improves the baroreceptor refle

10 ablated by treatment with the Ang II type 1 (AT1) receptor antagonist losartan.

11 th reflexes were blocked by an ANGII type 1 (AT1) receptor antagonist, losartan (20 microM).

12 bitor but not with an angiotensin II type 1 (AT1) receptor antagonist.

13 assessed the role of angiotensin II type 1 (AT1) receptor antagonists on inflammatory mechanisms inv

14 ory to the classic RAS Ang II/Ang II Type 1 (AT1) receptor axis.

15 o migraine prevention is angiotensin type 1 (AT1) receptor blockade.

16 ked by coadministration of the AngII type 1 (AT1) receptor blocker candesartan (10(-8) M).

17 ration of the angiotensin II (AngII) type 1 (AT1) receptor blocker candesartan elicited divergent ren

18 plasmic domain of the angiotensin II type 1 (AT1) receptor has recently been shown to interact with s

19 d monoclonal antibodies to the AngII type 1 (AT1) receptor have demonstrated an abundance of the AT1

20 med to determine whether angiotensin type 1 (AT1) receptor inhibition improves abnormal coronary vaso

21 ecent studies showed that the Ang II type 1 (AT1) receptor is also directly activated by mechanical f

22 noreactivity (IR) and to angiotensin type 1 (AT1) receptor mRNA in forebrain regions implicated in th

23 olved in the angiotensin II (Ang II) type 1 (AT1) receptor signaling, how AT1 receptors activate tyro

24 The type 1 (AT1) receptor that mediates most Ang II effects is upreg

25 The angiotensin-II type 1 (AT1) receptor, a prototypical class A G protein-coupled

26 Our group identified angiotensin II type 1 (AT1) receptor-associated protein (ATRAP) in a yeast two-

27 lls (VSMCs) inhibited angiotensin II type 1 (AT1) receptor-mediated tyrosine phosphorylation of STAT

28 lar remodeling, are mediated via its type 1 (AT1) receptor.

29 that the angiotensin (ang) II/ang II type-1 (AT1) receptor pathway may participate, together with the

30 giotensin system are mediated by the type-1 (AT1) receptor, and the functions of the type-2 (AT2) rec

31 ssion of the angiotensin II (Ang II) type-1 (AT1) receptor.

32 Ang II type 1 (AT1) receptors activate both conventional heterotrimeric

33 his regulation is mediated by Ang II type 1 (AT1) receptors and abolished by NADPH oxidase inhibitors

34 activation of cerebrovascular AngII type 1 (AT1) receptors by AngII.

35 giotensin II (ANGII) acting on ANGII type 1 (AT1) receptors in the solitary tract nucleus (NTS) depre

36 terious actions by activating Ang II type 1 (AT1) receptors on cerebral blood vessels and producing r

37 the immunoreactivity of angiotensin type 1 (AT1) receptors was colocalized with a presynaptic marker

38 (AngII), acting through angiotensin type 1 (AT1) receptors, exerts powerful effects on central auton

39 l importance of brain angiotensin II type 1 (AT1) receptors, we developed a novel transgenic mouse mo

40 This action was mediated by Ang II-type 1 (AT1) receptors.

41 In rodents, angiotensin (Ang) II type-1 (AT1) receptors exist as two pharmacologically identical

42 ffects of intravenous injection of CV-11974 (AT1 receptor antagonist) on the baroreflex control of re

43 tissue, EP promoted mRNA increases for ACE, AT1 receptor, and inflammatory mediators as well as decr

44 gonistic antibodies (AT1-AAs) could activate AT1 receptors, leading to an increased intracellular con

45 IgG from all preeclamptic patients activated AT1 receptors and increased intracellular free calcium.

46 I impairs functional hyperemia by activating AT1 receptors and inducing ROS production via a gp91phox

47 at maternal antibodies capable of activating AT1 receptors are likely to account for increased intrac

48 ve individuals had IgG capable of activating AT1 receptors.

49 Acute AT1 receptor blockade by candesartan reduced tubuloglome

50 sor test (CPT) and exercise before and after AT1 receptor blockade with intracoronary losartan (5 mg)

51 for 2 weeks, in particular reduced amygdala AT1 receptor and bed nucleus of the stria terminalis c-F

52 Inhibition by an AT1 receptor antagonist (losartan metabolite: E3174) or

53 p38MAPK and JNK by AngII was inhibited by an AT1 receptor antagonist, RNH6270 and EGF markedly activa

54 In CHF glomus cells, an AT1 receptor (AT1R) antagonist, L-158 809 (1 microM), al

55 Ca2+ by AT1-AAs was blocked by losartan, an AT1 receptor antagonist, and by a 7-amino-acid peptide t

56 Losartan, an AT1 receptor antagonist, and inhibitors of either mitoge

57 in the presence of PD123319 or losartan, an AT1 receptor blocker.

58 f WT AT1 receptor (AT1-WT; Tg-WT mice) or an AT1 receptor second intracellular loop mutant (AT1-i2m;

59 emonstrated that combination therapy with an AT1 receptor blocker and a vitamin D analog markedly ame

60 Similar changes of CXCR4, SDF-1, and AT1 receptor expression were found in Munich Wistar From

61 Normally, angiotensin and AT1 receptor are transiently up-regulated around the ren

62 transcriptional activity for bax, Aogen, and AT1 receptor.

63 erting enzyme inhibitor normalized CXCR4 and AT1 receptor expression on progenitors concomitant with

64 ction, mitogen-activated protein kinase, and AT1 receptor desensitization and internalization were no

65 hese responses were inhibited by PD98059 and AT1 receptor antagonist candesartan.

66 ribute to vascular dysfunction via LOX-1 and AT1 receptors during pregnancy.

67 cells were also double labelled for eNOS and AT1 receptors.

68 ssing cloned Kv7.2 + 7.3 heteromultimers and AT1 receptors studied under perforated patch clamp, angi

69 cts of the nonpeptide angiotensin II (AngII) AT1 receptor blocker candesartan on responses to AngII w

70 neurons, which endogenously express angioII AT1 receptors, application of angioII for 2 min produced

71 sartan is a potent and selective angiotensin AT1 receptor blocker that can induce both surmountable a

72 The angiotensin AT1 receptor expression and protein kinase C (PKC)-media

73 The angiotensin AT1 receptor has been shown to activate both ERK1/2 and

74 s vasoconstriction by activating angiotensin AT1 receptors.

75 nin-angiotensin system (RAS) and angiotensin AT1 receptors within the brain are also involved in the

76 Signaling through both angiotensin AT1 receptors (AT1R) and dopamine D1 receptors (D1R) mod

77 involve covalent crosslinking of angiotensin AT1 receptors by factor XIIIA transglutaminase, resultin

78 rray of kidney diseases, type 1 angiotensin (AT1) receptors are present on the immune cells that infi

79 To examine the role of type 1 angiotensin (AT1) receptors in glomerular inflammation associated wit

80 ical studies, activating type 1 angiotensin (AT1) receptors in T lymphocytes and myeloid cells blunts

81 is effect was AT1 receptor mediated, because AT1 receptor antagonists valsartan, candesartan, and los

82 Blocking AT1 receptors or PKC activity normalizes the increased p

83 Here we show that blocking AT1 receptors with losartan or inhibiting PKC with chele

84 Neurones double labelled for both AT1 receptors and eNOS comprised 23 +/- 5.4 % of the eNO

85 the modulation of the baroreflex control by AT1 receptor, the effects of intravenous injection of CV

86 on of TNF-alpha is suppressed or enhanced by AT1 receptor signaling in T lymphocytes or the distal ne

87 proinflammatory signaling events induced by AT1 receptor activation were attenuated when RAGE was de

88 -induced KDR expression was not inhibited by AT1 receptor blockade using candesartan.

89 augmentation of renal fibrosis instigated by AT1 receptor-deficient macrophages is mediated by IL-1 r

90 eduction in channel activity was mediated by AT1 receptor (AT1R) binding, because pretreatment of CCD

91 The cardiac dysfunction is prevented by AT1 receptor blockade.

92 ry circulation in DCM that are not shared by AT1 receptor antagonists.

93 esponse and TGF reactivity were unchanged by AT1 receptor blockade in euvolemic WKY.

94 how these different mechanisms activated by AT1 receptors affect growth and death of cardiac myocyte

95 L-type Ca2+ currents, an effect mediated by AT1 receptors and abolished by the ROS scavenger Mn(III)

96 II in the anesthetized mouse are mediated by AT1 receptors and that AT2 receptors do not modulate the

97 el AT1 receptor intracellular partner called AT1 receptor-associated protein (ATRAP) was identified,

98 n synthesis stimulated by both the canonical AT1 receptor agonist angiotensin II (AngII), and the arr

99 there is an enhanced contribution of central AT1 receptors to the maintenance of baseline BP in NSE-A

100 However, blockade of central AT1 receptors with ICV losartan caused significant falls

101 somatodendric and axonal profiles containing AT1 receptors.

102 Thus, arrestins coordinate AT1 receptor regulation of ERK1/2 and Akt activity and s

103 vates three major MAPKs via the G(q)-coupled AT1 receptor.

104 c calcium caused by activation of Gq-coupled AT1 receptors may mediate the renin-inhibitory effect of

105 biased for the Gq/11 pathway), and the D74N-AT1 receptor (biased for the beta-arrestin1 and -2 pathw

106 Simulations of the D74N-AT1 receptor revealed that the mutation stabilizes the r

107 ther stabilized the ground state of the D74N-AT1 receptor.

108 Ang II binding to AT2 receptors to determine AT1 receptor density in brain sections.

109 residual constrictor effect observed during AT1 receptor blockade and sensitive to PD 123319 appears

110 onse to Ang II stimulation, whereas the EGFR-AT1 receptor interaction was inhibited in the presence o

111 Our findings suggest that endogenous AT1 receptor-PKC activity is essential for presynaptic a

112 MDAR activity in the PVN, whether endogenous AT1 receptor-protein kinase C (PKC) activity mediates th

113 These results demonstrate that Ang II evokes AT1 receptor-mediated vasoconstriction and AT2 receptor-

114 phospholipids in CHO cells stably expressing AT1 receptors revealed that PIP2 and phosphatidylinosito

115 residual repertoire of systemic, extrarenal AT1 receptors is not sufficient to induce hypertension o

116 s were more numerous than those labelled for AT1 receptors.

117 The signaling transduction pathways for AT1 receptors include Gq/11-protein and protein kinase C

118 In contrast, dorsal root ganglia AT1 receptor mRNA content was significantly decreased in

119 Ang II) type 1 (AT1) receptor signaling, how AT1 receptors activate tyrosine kinases is not fully und

120 Combined angiotensin II type I (AT1) receptor blockade and ACE inhibition more completel

121 effect of the angiotensin II (AngII) type I (AT1) receptor blocker candesartan on renal vascular reac

122 at position 1,166 of the angiotensin type I (AT1) receptor gene.

123 dies directed against angiotensin II type I (AT1) receptors are also highly associated with preeclamp

124 ing, and this effect was inhibited by Ang II AT1 receptor (AT1R) blockade and in AT1aR-null mice.

125 low-protein diet increases glomerular Ang II AT1 receptor expression and decreases AT2 receptor expre

126 n ACE inhibitor but not by an angiotensin II AT1 receptor antagonist.

127 An increase in angiotensin II AT1 receptor mRNA at 3 days post-injury was also observe

128 this may be reversed by antagonizing ANG II AT1 receptors in the NTS.

129 ffect of systemic blockade of angiotensin II AT1 receptors by candesartan on the exaggerated tubulogl

130 -4) mol/l losartan, a type 1 angiotensin II (AT1) receptor antagonist.

131 Administration of the type 1 angiotensin II (AT1) receptor blocker candesartan (10 mg/kg) to untreate

132 y because stimulating type 1 angiotensin II (AT1) receptors in the kidney or circulating inflammatory

133 The Ang II/AT1 receptor pathway may participate, together with SDF-

134 Thus, targeting the Ang II/AT1 receptor/CXCR4 pathways may be beneficial in severe

135 iabetic state and leads to an angiotensin II/AT1 receptor-dependent systolic dysfunction and impaired

136 These endogenous functions of immune AT1 receptors temper the pathogenic actions of renal and

137 This was associated with an increase in AT1 receptor mRNA expression, a return of ACE activity b

138 Increased AT1 receptor expression in LP rat kidneys is consistent

139 We sought to determine if TNF-alpha-induced AT1 receptor upregulation alters fibroblast responsivene

140 Thus, TNF-alpha-induced AT1 receptor upregulation enhances Ang II-mediated funct

141 n cardiac fibroblasts with TNF-alpha-induced AT1 receptor upregulation, Ang II-stimulated [3H]proline

142 e effects of ATRAP on angiotensin II-induced AT1 receptor signaling reveals a moderate decrease in th

143 induce both surmountable and insurmountable AT1 receptor blockade and provide support for the hypoth

144 These data indicate that internalized AT1 receptors are processed via vesicles that resemble m

145 ect evidence that activation of intraluminal AT1 receptors by AngII exerts a substantial stimulatory

146 Evaluation of isolated AT1 receptor-deficient macrophages confirmed the propens

147 the pressor action of angiotensin II at its AT1 receptor.

148 ated from obstructed kidneys of mice lacking AT1 receptors solely on macrophages had heightened expre

149 In glomeruli with advanced lesions, AT1 receptor expression increased markedly, and the up-r

150 or the hypothesis that activation of luminal AT1 receptors by AngII present in the tubular fluid cont

151 Activation of luminal AT1 receptors stimulates tubular sodium reabsorption rat

152 tagamma as well as Galpha12 subunits mediate AT1 receptor coupling to tonic PLD activation via pp60(c

153 membrane and a reduction in plasma membrane AT1 receptors.

154 pe sampled by the WT-AT1 receptor, the N111G-AT1 receptor (constitutively active and biased for the G

155 the AngII-WT-AT1, N111G-AT1, and AngII-N111G-AT1 receptors revealed specific structural rearrangement

156 Neither AT1 receptor blockade nor ACE inhibition suppressed LTM.

157 nt indicates that activation of the neuronal AT1 receptor inhibits CGRP synthesis in the dorsal root

158 es of arrestin pathway-selective and neutral AT1 receptor ligands may translate into different pharma

159 to PD 123319 appears to be mediated by a non-AT1 receptor.

160 A novel AT1 receptor intracellular partner called AT1 receptor-a

161 Selected rats received the novel AT1 receptor blocker candesartan cilexetil (1.0 mg/kg pe

162 Activation analysis of AT1 receptor position 111 mutants by various Ang II posi

163 proteins that regulate different aspects of AT1 receptor physiology.

164 Mutant mice completely devoid of AT1 receptor fail to develop the renal pelvis and the ur

165 To evaluate the direct effects of AT1 receptor blockade on renal function in AngII-depende

166 estigated the acute and long-term effects of AT1 receptor inhibition on fear memory and baseline anxi

167 By counteracting the effects of AT1 receptor stimulation in the target organ, exogenous

168 to the potential therapeutic implications of AT1 receptor antagonists.

169 Inhibition of AT1 receptor-PKC activity in the hypothalamus reduces ar

170 Furthermore, levels of AT1 receptor mRNA and PKC-mediated NMDAR phosphorylation

171 PEG-catalase, suggesting a critical role of AT1 receptor and H(2)O(2) in this response(.) In contras

172 Here, we examined the actions of AT1 receptors on macrophages in progressive renal fibros

173 Thus, activation of AT1 receptors by Ang II or stretch specifically destabil

174 Although angiotensin II activation of AT1 receptors induces a significant increase in the leve

175 Angiotensin II, through the activation of AT1 receptors, promotes the recruitment to the plasma me

176 of HS rats (33%), and central antagonism of AT1 receptors (losartan) microinjected into the lateral

177 ated by either pharmacological antagonism of AT1 receptors or AT1A receptor deficiency.

178 Blockade of AT1 receptors partially reversed this change in MSNA dur

179 er, indicating an insurmountable blockade of AT1 receptors.

180 hemistry revealed widespread distribution of AT1 receptors in neurons throughout the CNS.

181 Furthermore, inhibition of AT1 receptors with candesartan cilexetil provides protec

182 Our findings suggest selective inhibition of AT1 receptors within the nephron as a promising interven

183 In contrast, knockout of AT1 receptors on kidney epithelial cells ameliorated the

184 Notably, knockout of AT1 receptors on T lymphocytes exacerbated the severity

185 one, despite a compensatory up-regulation of AT1 receptors and an augmented hypertensive response to

186 This study indicates that a key role of AT1 receptors on macrophages is to protect the kidney fr

187 that angiotensin II (Ang II) stimulation of AT1 receptors in proximal tubule cells induces the recru

188 mesenteric artery myocytes by stimulation of AT1 receptors linked to PLC.

189 We propose that stimulation of AT1 receptors with subsequent activation of NADPH oxidas

190 evious findings of a twofold upregulation of AT1 receptors in CRF colonic mucosa.

191 es hypertension primarily through effects on AT1 receptors in the kidney.

192 When angiotensin II or AT1 receptor is experimentally inhibited during the peri

193 ed substantial FRET between AKAP79 and M1 or AT1 receptors, and with the channels, but only weak FRET

194 tic inputs through activation of presynaptic AT1 receptors.

195 ation of the angiotensin II type 1 receptor (AT1) receptor.

196 exibility than previously believed regarding AT1 receptor activation and supporting the possibility o

197 We find that renal AT1 receptors are absolutely required for the developmen

198 urrently, the quantity of p53, Aogen, renin, AT1 receptor, and Bax was reduced in stretched myocytes

199 3 3'-UTR reporter activity and this requires AT1 receptors and NADPH oxidase.

200 est that in vivo, arrestin pathway-selective AT1 receptor agonists may promote cell growth or hypertr

201 The selective AT1 receptor blocker (ARB) losartan abrogated aneurysm p

202 developed an experimental model to separate AT1 receptor pools in the kidney from those in all other

203 rt for the hypothesis that there are "spare" AT1 receptors in the hindquarters vascular bed of the ca

204 (p < 0.01), and was inhibited by a specific AT1 receptor antagonist, Losartan (74 +/- 14%).

205 fibrosis and found that macrophage-specific AT1 receptor deficiency exacerbates kidney fibrosis indu

206 We tested the hypothesis that AT1 receptor-agonistic antibodies (AT1-AAs) could activa

207 These data suggest that AT1 receptor antagonism enhances the extinction of fear

208 duced lung fibrosis in mice and suggest that AT1 receptor signaling is required for BLEO-induced apop

209 ivated by mechanical forces, suggesting that AT1 receptors play an important role in mediating load-i

210 The AT1 receptor antagonist losartan (2 microm, n = 6) aboli

211 The AT1 receptor engages and activates several signaling pat

212 The AT1 receptor polymorphism did not influence responses to

213 The AT1 receptor-mediated ERK/p38 MAP kinase signaling pathw

214 eptide angiotensin II (Ang II) activates the AT1 receptor through an induced-fit mechanism.

215 In addition, the AT1 receptor blocker irbesartan was evaluated for its ab

216 The MMP inhibitor GM6001 and the AT1 receptor antagonist Losartan inhibited these effects

217 otensin-converting enzyme inhibitors and the AT1 receptor antagonists, unblocked aldosterone levels r

218 nses to AngII were long in duration, and the AT1 receptor blocker had little effect on baseline press

219 ity to angiotensinogen (Aogen), bax, and the AT1 receptor was determined in left ventricular myocytes

220 ted gene expression is inhibited by both the AT1 receptor blocker losartan and by spironolactone, but

221 evoked Icat1 and Icat2 were inhibited by the AT1 receptor antagonist losartan and the phospholipase C

222 el Ca2+-dependent pathway was blocked by the AT1 receptor antagonist losartan, or by including guanos

223 The effect of Ang II was abolished by the AT1 receptor antagonist losartan.

224 se data position RAGE transactivation by the AT1 receptor as a target for vasculoprotective intervent

225 ffects of AngII were inhibited by 88% by the AT1 receptor blocker candesartan in renal SMC.

226 of mTOR-dependent protein translation by the AT1 receptor using HEK293 and primary vascular smooth mu

227 These effects of AII are mediated by the AT1 receptor.

228 To correlate the AT1 receptor blockage to anticancer effects, VEGF levels

229 This study supports a role for the AT1 receptor signaling pathway in the pathogenesis of PT

230 f the AT2 receptor were substituted into the AT1 receptor were used to investigate the activation mec

231 pendent activation when substituted into the AT1 receptor.

232 cells expressing AT1-Y319E, which mimics the AT1 receptor phosphorylated at Tyr-319.

233 , neither the ACE inhibitor ramipril nor the AT1 receptor blocker telmisartan affected lung or kidney

234 proliferation in vitro via activation of the AT1 receptor and involves the autocrine action of TGF-be

235 Thus, MEKK3 functions downstream of the AT1 receptor and is essential for calcineurin/NFAT activ

236 o the orthosteric ligand binding site of the AT1 receptor and promoting co-sequestration of AT1-B2 he

237 n operates between the residue Asn111 of the AT1 receptor and Tyr4 of Ang II.

238 Coadministration of the AT1 receptor antagonist losartan (1 to 1000 ng) elicited

239 Administration of the AT1 receptor antagonist telmisartan 1 hour post-injury s

240 The high tolerability of the AT1 receptor blocker candesartan warrants further studie

241 mpletely reversed by coadministration of the AT1 receptor blocker candesartan.

242 Activation of the AT1 receptor by angiotensin II (Ang II) triggered transa

243 examined the structural requirements of the AT1 receptor for transactivation of the epidermal growth

244 that underlie functional selectivity of the AT1 receptor in human embryonic kidney 293 cells.

245 eventh transmembrane-spanning domains of the AT1 receptor involved in the intrareceptor activation me

246 In summary, Tyr-319 of the AT1 receptor is phosphorylated in response to Ang II and

247 otein coupling, the carboxyl terminus of the AT1 receptor is required for activation of Src.

248 ceptor have demonstrated an abundance of the AT1 receptor not only on the luminal surface of proximal

249 Although both reduce stimulation of the AT1 receptor, ARB lack the kinin-potentiating effects of

250 Similarly, levels of the AT1 receptor, but not the AT2 receptor, were significant

251 Phe8 of Ang II with Asn111 and His256 of the AT1 receptor, respectively, are essential for agonism.

252 ssion is mediated by AngII activation of the AT1 receptor, whereas an AT1-independent mechanism is op

253 eNOS-positive cells and 57 +/- 9.2 % of the AT1 receptor-positive cells.

254 rat by down-regulating the expression of the AT1 receptor.

255 tion of the second extracellular loop of the AT1 receptor.

256 -induced GRK-mediated phosphorylation of the AT1 receptor.

257 of six different signaling modalities of the AT1 receptor.

258 ssociated with distinct conformations of the AT1 receptor.

259 inea pig hearts treated with BILA2157 or the AT1 receptor antagonist EXP3174.

260 of [Sar(1),Ile(4), Ile(8)]-AngII require the AT1 receptor and result from arrestin-dependent co-inter

261 scopic immunohistochemistry we find that the AT1 receptor in the thoracic spinal cord is located on n

262 Here, we report that the AT1 receptor preformed a heteromeric complex with the re

263 activates PAI-1 gene expression through the AT1 receptor and involves the calcium-dependent activati

264 Thus, the AT1 receptor mediates downstream signaling mechanisms th

265 etermined by the sensitivity of Jprox to the AT1 receptor antagonist, losartan.

266 timulation, betaarrestin is recruited to the AT1 receptor, leading to receptor desensitization.

267 g the carboxyl end are unable to bind to the AT1 receptor, leading to the formation of prominent peri

268 both in vivo and in vitro conditions via the AT1 receptor and intracellular extracellular regulated k

269 glin is upregulated in CFs by Ang II via the AT1 receptor and modulates profibrotic effects of Ang II

270 hat angiotensin II up-regulates LARG via the AT1 receptor, and this up-regulation is signaled via the

271 Treatment with the AT1 receptor blocker, irbesartan rescued the systolic dy

272 EGFR interacted with the AT1 receptor but not with AT1-Y319F in response to Ang I

273 SMC and was phosphorylated by Ang II through AT1 receptor.

274 This study shows that AngII acts through AT1 receptors to stimulate [Ca2+]i by a predominant acti

275 Because the response to AT1 receptor blockade was very similar to the response i

276 emodynamic and sodium excretory responses to AT1 receptor blockade in hypertensive rats, depending on

277 ignals produced by angiotensin II binding to AT1 receptors.

278 Studies using carboxyl terminal-truncated AT1 receptors indicated that the amino acid sequence bet

279 Overexpression of wild type AT1 receptor in cardiac fibroblasts enhanced Ang II-indu

280 acies and potencies similar to the wild-type AT1 receptor.

281 n-converting enzyme activity and upregulated AT1 receptors and angiotensin-converting enzyme in P1 EC

282 the pathogenic actions of renal and vascular AT1 receptors during hypertension.

283 Inhibition of the coronary vascular AT1 receptors in patients with atherosclerosis improves

284 ation and ER stress in adipocytes mainly via AT1 receptor, possibly mediated by miR-30 family, -708-5

285 utable to elevated superoxide production via AT1 receptor activation of NADPH oxidase.

286 hibition of skeletal muscle regeneration via AT1 receptor-dependent suppression of SC Notch and MyoD

287 s macula densa basolateral Na/H exchange via AT1 receptors and therefore may affect tubuloglomerular

288 modulator of renal cortical oxygenation via AT1 receptors.

289 confirmed that Ang II-induced DNA damage was AT1 receptor-mediated, via the induction of ROS.

290 This effect was AT1 receptor mediated, because AT1 receptor antagonists

291 When AT1 receptors are eliminated from the kidney, the residu

292 uli affected by early-stage lesions, whereas AT1 receptor expression could not be detected.

293 Whether AT1 receptor blockade will provide long-term therapeutic

294 Whether AT1 receptor blockade with losartan improves exercise ca

295 he aim of this study is to determine whether AT1 receptor (AT1R) contributes to production of inflamm

296 This explains why AT1 receptor blockers (ARBs) and inhibitors of Ang II sy

297 was completely inhibited by co-infusion with AT1 receptor antagonist, candesartan.

298 e with cardiac-specific overexpression of WT AT1 receptor (AT1-WT; Tg-WT mice) or an AT1 receptor sec

299 a preference for the ground state of the WT-AT1 receptor compared with AngII.

300 e conformational landscape sampled by the WT-AT1 receptor, the N111G-AT1 receptor (constitutively act