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 NTS can depress the baroreceptor re

4 AT1 receptors were more abundant than AT2 receptors in t

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

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

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

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

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

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

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

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

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

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

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

16 effects were prevented by the ANGII type 1 (AT1) receptor blocker losartan.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

46 ve individuals had IgG capable of activating AT1 receptors.

47 Acute AT1 receptor blockade by candesartan reduced tubuloglome

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

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

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

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

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

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

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

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

56 Administration of an AT1 receptor antagonist, losartan, also significantly in

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

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

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

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

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

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

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

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

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

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

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

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

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

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

71 s vasoconstriction by activating angiotensin AT1 receptors.

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

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

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

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

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

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

78 p53 DNA binding to angiotensinogen (Aogen), AT1 receptor, and Bax was markedly down-regulated by IGF

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

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

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

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

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

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

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

86 The cardiac dysfunction is prevented by AT1 receptor blockade.

87 of autoregulatory behavior was prevented by AT1 receptor blockade.

88 Inhibition of the response by AT1 receptor antagonist suggests mediation by the AT1B r

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

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

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

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

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

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

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

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

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

98 somatodendric and axonal profiles containing AT1 receptors.

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

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

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

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

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

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

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

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

107 evels for euvolemic animals, persists during AT1 receptor blockade in both groups of rats.

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

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

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

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

112 ss of 18 kDa, which we have named ATRAP (for AT1 receptor-associated protein).

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

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

115 ased levels of angiotensin II resulting from AT1 receptor blockade.

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

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

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

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

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

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

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

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

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

125 ally active antagonist of the angiotensin II AT1 receptor subtype with potential efficacy in heart fa

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

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

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

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

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

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

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

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

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

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

136 Increased AT1 receptor expression in LP rat kidneys is consistent

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

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

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

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

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

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

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

144 Blockade of intrarenal AT1 receptors elicited significant increases in GFR, ren

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

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

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

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

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

150 Activation of luminal AT1 receptors stimulates tubular sodium reabsorption rat

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

152 membrane and a reduction in plasma membrane AT1 receptors.

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

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

155 Neither AT1 receptor blockade nor ACE inhibition suppressed LTM.

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

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

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

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

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

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

162 proteins that regulate different aspects of AT1 receptor physiology.

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

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

165 enal vasodilation and natriuretic effects of AT1 receptor blockade.

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

170 al studies have demonstrated an abundance of AT1 receptors on the luminal surface of proximal and dis

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

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

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

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

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

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

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

178 er, indicating an insurmountable blockade of AT1 receptors.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

193 tic inputs through activation of presynaptic AT1 receptors.

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

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

196 Northern blot analysis showed that renal AT1 receptor mRNA levels (AT1 mRNA/18 rRNA) were signifi

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 f heterotrimeric G proteins, indicating that AT1 receptor-PLD coupling requires pertussis toxin-insen

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

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

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

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

212 The AT1 receptor engages and activates several signaling pat

213 The AT1 receptor polymorphism did not influence responses to

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

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

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

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

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

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

220 Coexpression of Kv2.2 and the AT1 receptor in Xenopus oocytes demonstrated an Ang II-i

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

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

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

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

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

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

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

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

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

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

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

232 pendent activation when substituted into the AT1 receptor.

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

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

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

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

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

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

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

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

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

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

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

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

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

254 of six different signaling modalities of the AT1 receptor.

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

256 ssociated with distinct conformations of the AT1 receptor.

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

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

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

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

261 Although it is generally agreed that the AT1 receptor subtype mediates AngII-induced sodium-bicar

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

263 Thus, the AT1 receptor mediates downstream signaling mechanisms th

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

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

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

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

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

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

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

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

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

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

274 Galpha12 may also contribute to AT1 receptor-PLD coupling because electroporation of ant

275 profen on the renal and systemic response to AT1 receptor blockade in conscious rats developing spont

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

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

278 ignals produced by angiotensin II binding to AT1 receptors.

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

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

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

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

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

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

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