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1 ((13)C(6)-ochratoxin A), and an octapeptide (angiotensin II).
2 ectomy) and a hypertension model (induced by angiotensin II).
3 to myofibroblasts in the presence of Ang II (angiotensin II).
4 of the most potent vasoconstrictors, peptide angiotensin II.
5 s suppressed the vasoconstrictor response to angiotensin II.
6 blast transformation induced by TGFbeta1 and angiotensin II.
7 hancement, 100 picomole) in the detection of angiotensin II.
8 ility to remodel cardiac tissue and generate angiotensin II.
9 thout influencing the hypertensive effect of angiotensin II.
10 s is a systematic review of the safety of IV angiotensin II.
11 ce with a combination of a high-fat diet and angiotensin II.
12 f post-pneumonectomy vasoplegia managed with angiotensin II.
13 between ACE and ACE2 result in an unopposed angiotensin II.
15 ipoprotein E knockout mice were infused with angiotensin II (0.72 mg.kg(-1).d(-1) subcutaneous) for 2
16 nsion, wild-type NMRI mice were infused with angiotensin II (1.44 mg.kg(-1).d(-1) subcutaneous) for 1
17 ipumps with a continuous infusion of Ang II (angiotensin II; 1000 ng/[kg.min]) to induce AAAs were im
19 e to 2 weeks of continuous administration of angiotensin II, a profibrotic stimulus that drives patho
21 actors implicated in muscle atrophy, such as angiotensin-II, activin and Acvr2b, in SIRT6 depleted ce
23 of intrakidney paracrine hormones including angiotensin II, aldosterone, and endothelin-1 (ET-1) tha
24 these adaptive responses; reduces levels of angiotensin II, aldosterone, and ET-1; reduces ammoniage
25 activated in heart failure (norepinephrine, angiotensin II, aldosterone, and neprilysin) impair insu
26 activity repressed by albumin, high glucose, angiotensin II, aldosterone, cisplatin and lipopolysacch
28 wed an elevated contractile response to 5 nM angiotensin II and a loss of acetylcholine (ACh)-mediate
29 levels of anti-natriuretic hormones, such as angiotensin II and aldosterone; and adipokines, particul
30 injury (post-AKI) rats were stimulated with angiotensin II and elevated Na+ (10-7 M/170 mM) in vitro
31 damental unit of zG layer activity evoked by angiotensin II and highlight a novel role for the rosett
32 ctor (HIF)-1alpha and -2alpha in response to angiotensin II and hypoxia, respectively, which drive VE
33 orescence in response to exogenously applied angiotensin II and III, but not other common neurotransm
36 rch is warranted to determine the utility of angiotensin II and to better understand it effects on th
38 ress, and hypertrophy and attenuates Ang II (angiotensin II) and deoxycorticosterone acetate-salt ind
39 received a study intervention (163 received angiotensin II, and 158 received placebo) and were inclu
40 ore age 60, blunted hypertensive response to angiotensin II, and a leftward shift in pressure natriur
41 o-HDL cholesterol ratio, C-reactive protein, angiotensin II, and albuminuria reduction and with incre
42 timulated cGMP generation, suppressed plasma angiotensin II, and reduced cardiac filling pressures wi
44 istration of vasoconstrictive agents such as angiotensin II (Ang II) and phenylephrine results in an
46 K mutation in mice subjected to high salt or angiotensin II (Ang II) as models of hypertension and in
48 oconstrictor and a proinflammatory mediator, angiotensin II (Ang II) is considered a potential link b
52 um influx, and we have previously shown that angiotensin II (Ang II) via canonical transient receptor
54 nsin-converting enzymes (ACEs) ACE and ACE2, angiotensin II (Ang II), Ang-(1-7), and receptors AT1 an
55 rmone of the renin-angiotensin system (RAS), angiotensin II (Ang II), is involved in several human di
56 rbate vascular senescence and progression of angiotensin II (Ang II)-induced AAA by facilitating reac
59 ing pathways involved in the effect of LC on angiotensin II (Ang II)-induced NADPH oxidase activation
61 ion of collagen alpha1(I) gene expression in angiotensin II (Ang II)-stimulated cardiac fibroblasts.
63 cally transforms Ang-I to a secondary ligand angiotensin II (Ang-II) that has the potential to bind i
64 This study tests a direct role of IgE in angiotensin-II (Ang-II) perfusion- and peri-aortic CaCl(
65 converting enzyme 2 (ACE2) promotes the ACE/angiotensin-II (Ang-II)/angiotensin type 1 receptor (AT1
66 as profiles: the balanced endogenous agonist angiotensin II (AngII) and two strongly beta-arrestin-bi
67 NaCl concentrations and the peptide hormone angiotensin II (AngII) are two major neurohumoral signal
70 ding partners and that activation of AT1R by angiotensin II (ANGII) elicits beta-arrestin-dependent i
71 E knockout (ApoE-KO) mice were infused with angiotensin II (AngII) for 28 days to induce AAA formati
78 esponse to TGF-beta, increased expression of angiotensin II (AngII) type 1 receptor (Agtr1a), enhance
82 udies have shown that serelaxin requires the angiotensin II (AngII) type 2 receptor (AT(2)R) to ameli
84 e RAS are mediated by the vasoactive hormone angiotensin II (AngII) via two receptor subtypes, AT1R (
85 ocytes and tubular epithelia and metabolizes angiotensin II (AngII), a peptide known to promote glome
89 ntity during homeostasis, and in response to angiotensin-II (AngII)-induced arterial inflammation.
92 associated with higher risk for AMI; whereas angiotensin-II-antagonists, calcium-channel blockers, an
94 and hemodynamic responses to an infusion of angiotensin II (assessment of intrarenal renin-angiotens
95 nction in rats, and the impact of intrarenal angiotensin II AT(1) receptor blockade using candesartan
98 ind that increased complex formation between angiotensin II AT1 and bradykinin B2, two G protein-coup
101 tensin-converting enzyme or the receptor for angiotensin II attenuated VEGF-mediated relaxation of th
102 ensin-converting enzyme) inhibitors and ANG (angiotensin) II blockers, neprilysin inhibitors, and ald
103 In euvolemic rats, the dipsogenic hormone angiotensin II, but not the orexigenic hormone ghrelin,
104 where these tumor cells autocrinely produce angiotensin II by a chymase-dependent rather than an ang
105 critical role of hypoxia in producing local angiotensin II by a lactate-chymase-dependent mechanism
108 t Shock) trial for renin, angiotensin I, and angiotensin II concentrations before the start of admini
111 echanistically, we found that Plk1 regulated angiotensin II-dependent activation of RhoA and actomyos
113 explore the repurposing of drugs that target angiotensin II-dependent NFkappaB signaling pathways to
115 included number of subjects, comorbidities, angiotensin II dose and duration, pressor effects, other
117 Here we demonstrate that within the rosette, angiotensin II evokes periodic Ca(v)3-dependent calcium
120 mples from patients enrolled in the ATHOS-3 (Angiotensin II for the Treatment of High-Output Shock) t
123 nd point was reached by more patients in the angiotensin II group (114 of 163 patients, 69.9%) than i
124 ere reported in 60.7% of the patients in the angiotensin II group and in 67.1% in the placebo group.
125 occurred in 75 of 163 patients (46%) in the angiotensin II group and in 85 of 158 patients (54%) in
126 more severe dysfunction) was greater in the angiotensin II group than in the placebo group (-1.75 vs
127 s systematic review supports the notion that angiotensin II has an acceptable safety profile for use
129 (transforming growth factor beta) and AngII (angiotensin II), have been well characterized, less unde
130 ssed by acetylcholine, albumin, aldosterone, angiotensin II, high glucose, cisplatin and lipopolysacc
131 otensin peptides revealed elevated levels of angiotensin II, III, IV, and 1-5 in DPP3(-/-) mice, wher
132 was fatal in 55 of 115 patients treated with angiotensin II in case studies, cohort studies, and one
134 hanism and highlight the importance of local angiotensin II in regulating radioresistance of hypoxic
137 The levels of ET-1(endothelin-1) and Ang II (Angiotensin II) in the plasma were measured by an enzyme
138 hermore, telemetry studies showed that while angiotensin II increased blood pressure acutely in all a
140 c-expressing myeloid cells mitigates Ang II (angiotensin II)-induced hypertension by limiting renal T
141 ersus male (XY) sex chromosome complement on angiotensin II-induced AAA formation and rupture in phen
143 a multifaceted therapeutic effect to prevent angiotensin II-induced cardiac dysfunction by improving
144 BMMO-derived HuR-deficient exosomes inhibits angiotensin II-induced cardiac fibrosis response and pre
150 In animal models of nitrate tolerance and angiotensin II-induced hypertension, decreased vasodilat
151 loid-specific Nox2 deletion had no effect on angiotensin II-induced hypertension, which, however, was
154 the hypoxia-inducible factor complex, during angiotensin II-induced hypertensive nephropathy provided
155 NRP1 contributes to protection from low-dose angiotensin II-induced increases in blood pressure.
156 ealed that VEGFCc156s specifically modulated angiotensin II-induced inflammatory responses in cardiac
159 Oxidized LDL (a LOX-1 ligand) increased angiotensin II-induced vasoconstriction in STBEV-incubat
162 were abrogated in regulatory T cell-depleted angiotensin II-infused mice, suggesting the effect is re
165 on coculture with dendritic cells from Ang (angiotensin) II-infused mice, were reduced in denervated
171 sporadic AAD induced by a high-fat diet and angiotensin II infusion, ADAMTS-4 deficiency (Adamts-4-/
172 , transverse aortic constriction banding and angiotensin II infusion, and a genetic model of Etv1 car
174 level, they were more sensitive to low-dose angiotensin II infusion-induced increases in blood press
177 e subjected to pressure overload by means of angiotensin-II infusion or transversal aortic constricti
180 asma renin activity drawn immediately before angiotensin II initiation was 40 ng/mL/hr (normal, 0.6-3
182 dentified ACE2 as the main enzyme converting angiotensin II into angiotensin-(1-7) in human cerebrosp
184 e A inhibitor preventing conversion of brain angiotensin-II into angiotensin-III, in BP lowering in a
190 perivascular tissues in response to Ang II (angiotensin II)-mediated hypertension, miR-214 showed th
192 endogenous and synthetic agonists inhibited angiotensin II-mediated G-protein-associated second mess
193 unappreciated roles for Micu2 in regulating angiotensin II-mediated hypertensive responses that are
194 itro findings were confirmed in vivo with an angiotensin II-mediated murine model of cardiac fibrosis
195 protein-coupled receptor agonists, including angiotensin II or bombesin, induced rapid and persistent
196 ations before the start of administration of angiotensin II or placebo and after 3 hours.Measurements
198 myocyte pathological hypertrophy induced by Angiotensin II, phenylephrine, and isoproterenol, but di
201 angiotensin-converting enzyme 2, the type 2 angiotensin II receptor (AT(2)R), the proto-oncogene Mas
208 giotensin-converting enzyme inhibitor (ACEI)/angiotensin II receptor blocker (ARB), angiotensin recep
209 laboratory monitoring after ACE inhibitor or angiotensin II receptor blocker initiation was not assoc
210 ut more expensive, heart failure medication (angiotensin II receptor blocker neprilysin inhibitor).
211 f angiotensin-converting enzyme inhibitor or angiotensin II receptor blocker therapy and glucose-lowe
212 51 matched pairs initiating ACE inhibitor or angiotensin II receptor blocker therapy between January
213 the 30 days after starting ACE inhibitor or angiotensin II receptor blocker therapy were matched 1:1
215 o angiotensin-converting enzyme inhibitor or angiotensin II receptor blocker treatment, is a potentia
216 [angiotensin-converting enzyme] inhibitor or angiotensin II receptor blocker) and a newer, but more e
217 otensin-converting enzyme inhibitor) or ARB (angiotensin II receptor blocker), be switched to sacubit
219 ensin-converting enzyme inhibitors (ACEi) or angiotensin II receptor blockers (ARB) during hospitaliz
220 giotensin-converting enzyme (ACE) inhibitors/angiotensin II receptor blockers (ARB), beta-blockers an
221 ensin-converting enzyme inhibitors (ACEI) or angiotensin II receptor blockers (ARBs) does not increas
222 ensin-converting enzyme (ACEs) inhibitors or angiotensin II receptor blockers (ARBs) in CKD is lackin
223 oV-2 positive test result compared to use of angiotensin II receptor blockers (OR = 0.70, 95% CI 0.54
226 sed case-control study indicates that use of angiotensin II receptor blockers might be associated wit
228 reatitis and 61,637 controls, current use of angiotensin II receptor blockers was followed by a decre
229 angiotensin-converting enzyme inhibitors or angiotensin II receptor blockers), avoidance of potentia
231 titis, by degree of severity, among users of angiotensin II receptor blockers, as compared to non-use
232 angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers, beta-blockers, thiazid
233 e collected from patients, with attention to angiotensin II receptor blockers, such as olmesartan, al
235 induced ER stress and inflammation, whereas angiotensin II receptor inhibitor, telmisartan reduced R
236 d type, P = 7.8 x 10(-40)), which suppresses angiotensin II receptor signaling via allosteric transin
237 data analysis identified one important gene, angiotensin II receptor type 1 (AGTR1), in the Ca2+/AT-I
238 -2 binding, ACE2 downregulation enhances the angiotensin II receptor type 1 (AT(1) R) axis associated
239 Substantial evidence indicates that the angiotensin II receptor type 1 (AT1 R) is inherently mec
241 ay, we characterize a GPCR-TRP channel pair, angiotensin II receptor type 1 (AT1R), and transient rec
242 027, a beta-arrestin-1-biased agonist of the angiotensin II receptor type 1 (AT1R), stimulates acute
244 induced sympathoexcitation is independent of angiotensin II receptor type 1, oxytocin, ionotropic glu
245 cation of Telmisartan (an antagonist for the angiotensin II receptor) through copper-mediated C-H ami
246 0067, a beta-arrestin 2-biased ligand of the angiotensin II receptor, or losartan, an angiotensin II
248 ngiotensin-I converting enzyme inhibitors or angiotensin-II receptor type 1 blockers may be less effe
254 Activation of either AT1 Ra or AT1 Rb with angiotensin II stimulates TRPM4 currents in cerebral art
257 e ACE2, leading to toxic overaccumulation of angiotensin II that induces acute respiratory distress s
260 nsors by allowing the short cationic peptide angiotensin II to be electrophoretically driven through
261 2 cleaves many biological substrates besides angiotensin II to control vasodilatation and vascular pe
262 treatment in hypertrophy samples, including angiotensin II-treated adult cardiac fibroblasts and ren
263 tration of small-molecule Plk1 inhibitors to angiotensin II-treated mice led to reduced arterial fitn
264 sets from transverse aortic constriction and angiotensin II-treated mice showed a high Pearson correl
265 eatment model of AAA in C57BL6 (WT) mice and Angiotensin II treatment model in ApoE(-/-) mice were us
266 s and shifts in cellular communication after angiotensin II treatment that promote the development of
269 (AGT), angiotensin-converting enzyme (ACE), angiotensin II type 1 receptor (AGTR1), and aldosterone
270 hese mice had increased renal expressions of angiotensin II type 1 receptor (AT(1) R), NADPH oxidase
271 this work, we present crystal structures of angiotensin II type 1 receptor (AT1R) (2.7 to 2.9 angstr
276 track activation and internalization of the angiotensin II type 1 receptor and the beta2 adrenocepto
277 aintained despite RVLM pretreatment with the angiotensin II type 1 receptor antagonist losartan, the
278 tics of graft injury in the presence of anti-angiotensin II type 1 receptor antibody (AT1R-Ab) and an
280 VLM of normotensive rats is not mediated via angiotensin II type 1 receptor, oxytocin, ionotropic glu
282 occurs selectively on neurons, and neuronal angiotensin II type 1 receptors are indispensable to thi
284 system and ADAM17, we generated mice lacking angiotensin II type 1 receptors specifically on neurons.
286 havioral approaches, we examined the role of angiotensin II type 2 receptor (AT(2)R) in fear-related
290 0 to 4 of 2009 with known HLA DSA status for angiotensin II type-1 receptor and endothelin-1 type A r
291 HLA antibodies, including antibodies against angiotensin-II type 1 receptor, did not contribute to ri
292 ], Rho guanine nucleotide exchange factor 6, angiotensin-II type 1 receptor, endothelin type A recept
293 were made hypertensive by administration of angiotensin II via osmotic mini-pumps and blood pressure
297 Studies in which human subjects received IV angiotensin II were selected whether or not safety was d
298 ation events by altering the balance between angiotensin II, which activates angiotensin receptor typ
300 angiotensin I to the potent vasoconstrictor angiotensin II while simultaneously halting the NEP-depe
301 wall shear stress, and exogenous sources of angiotensin II, with particular interest in mouse models