ライフサイエンスコーパス: angiotensin

1 -converting enzyme 2 (ACE2) and its product, angiotensin 1-7 (Ang-[1-7]), are important negative regu

2 s administration of AT2 receptor agonists or angiotensin 1-7 analogs may similarly limit inflammatory

3 the G-protein-coupled receptor (GPCR) MasR, angiotensin-(1-2) was found to signal via another GPCR,

4 and neprilysin-derived degradation products angiotensin-(1-4), angiotensin-(5-7), and angiotensin-(3

5 In neprilysin-deficient mouse islets, angiotensin-(1-7) and neprilysin-derived degradation pro

6 Studies show that generation of angiotensin-(1-7) by ACE2 and its binding to the Mas rec

7 gs warrant caution for the concurrent use of angiotensin-(1-7) compounds and neprilysin inhibitors as

8 e main enzyme converting angiotensin II into angiotensin-(1-7) in human cerebrospinal fluid.

9 ressed islet peptidase, neprilysin, degrades angiotensin-(1-7) into several peptides.

10 In conclusion, in islets, intact angiotensin-(1-7) is not the primary mediator of benefic

11 pression is sparse, its inhibition abrogates angiotensin-(1-7)-mediated GSIS.

12 r of beneficial effects ascribed to the ACE2/angiotensin-(1-7)/MasR axis.

13 ts angiotensin-(1-4), angiotensin-(5-7), and angiotensin-(3-4) failed to enhance GSIS.

14 ived degradation products angiotensin-(1-4), angiotensin-(5-7), and angiotensin-(3-4) failed to enhan

15 explore the repurposing of drugs that target angiotensin action to improve the treatment of AGTR1-exp

16 st, possibly because of the ability of renin-angiotensin activity to escape from suppression during l

17 ith use of certain medications such as renin angiotensin aldosterone inhibitors.

18 Renin-angiotensin aldosterone system (RAAS) inhibitors signifi

19 sidual albuminuria during single-agent renin-angiotensin-aldosterone blockade is accompanied by impro

20 A therapeutic agent that acts on the renin-angiotensin-aldosterone pathway, such as an angiotensin-

21 giotensin II (assessment of intrarenal renin-angiotensin-aldosterone system [RAAS]) were measured bef

22 on strategies, steroid minimization or renin-angiotensin-aldosterone system blockade result in better

23 SNPs at key renin-angiotensin-aldosterone system genes associate with syst

24 Renin-angiotensin-aldosterone system genes have been inconsist

25 mbination with other inhibitors of the renin-angiotensin-aldosterone system increases the risk of hyp

26 tor group versus 69.7 mm Hg in the non-renin-angiotensin-aldosterone system inhibitor group (p = 0.29

27 ssure at 6 hours was 72.2 mm Hg in the renin-angiotensin-aldosterone system inhibitor group versus 69

28 horts: 1) patients who were on chronic renin-angiotensin-aldosterone system inhibitor therapy as outp

29 nd 2) patients who were not on chronic renin-angiotensin-aldosterone system inhibitor therapy as outp

30 eiving vasopressin who were on chronic renin-angiotensin-aldosterone system inhibitor therapy versus

31 eiving vasopressin who were on chronic renin-angiotensin-aldosterone system inhibitor therapy with th

32 ng vasopressin who were not on chronic renin-angiotensin-aldosterone system inhibitor therapy.

33 dependent associations between age and renin-angiotensin-aldosterone system physiology.

34 Abnormal activity of the renin-angiotensin-aldosterone system plays a causal role in th

35 Tetralogy of Fallot: Inhibition of the Renin-Angiotensin-Aldosterone System) is an investigator-initi

36 ndothelial cells and by regulating the renin-angiotensin-aldosterone system, adiposity, energy expend

37 omeostasis includes suppression of the renin-angiotensin-aldosterone system, pressure natriuresis, an

38 ce exhibited similar activation of the renin-angiotensin-aldosterone system, whereas only dKO mice di

39 nd AT2R serve as key components of the renin-angiotensin-aldosterone system.

40 ronic (n = 59) and acute (n = 42) HF, plasma angiotensin analysis was performed using a unique liquid

41 -converting activities involved in the renin-angiotensin and the apelinergic systems, respectively.

42 ation of the biologically potent octapeptide angiotensin Ang II-(1-8) is mediated by the activities o

43 We aimed to determine whether angiotensin (Ang) II caused kinetic changes in gammadelt

44 cells (PECs)/progenitor cells, and that the angiotensin (ang) II/ang II type-1 (AT1) receptor pathwa

45 The angiotensin (ANG)-(1-7)/Mas receptor (MasR) pathway acti

46 The renin-angiotensin system (RAS) and angiotensin AT1 receptors within the brain are also invo

47 In preclinical studies, activating type 1 angiotensin (AT1) receptors in T lymphocytes and myeloid

48 olase PP for 1h (STP-C1) had the most potent angiotensin converting enzyme (ACE) and dipeptidyl pepti

49 lure with reduced ejection fraction, such as angiotensin converting enzyme (ACE) inhibitors, angioten

50 e Pinto bean peptides with alpha-amylase and angiotensin converting enzyme (ACE) inhibitory activitie

51 on with enhanced BP, decreased expression of angiotensin converting enzyme 2, and increased expressio

52 protein with approximately 50% homology with angiotensin converting enzyme 2, but without a catalytic

53 ified on QiShenYiQi Pills using thrombin and angiotensin converting enzyme as "quality biomarkers".

54 e, primary renal disease classification, and angiotensin converting enzyme inhibitor or angiotensin r

55 ioedema, hereditary angioedema type III, and angiotensin converting enzyme inhibitor-induced angioede

56 sin II by a chymase-dependent rather than an angiotensin converting enzyme-dependent mechanism.

57 To assess the effect of early angiotensin-converting enzyme (ACE) inhibitor therapy in

58 n reported to decrease time-to-resolution of angiotensin-converting enzyme (ACE) inhibitor-associated

59 Angiotensin-converting enzyme (ACE) inhibitors/angiotens

60 SNPs) at renin (REN), angiotensinogen (AGT), angiotensin-converting enzyme (ACE), angiotensin II type

61 Angiotensin-converting enzyme 2 (ACE2) and its product,

62 The conversion is catalyzed by angiotensin-converting enzyme 2 and other enzymes that s

63 was lower in fetal growth restriction in an angiotensin-converting enzyme 2 knockout mouse model cha

64 tory diagnostic biomarkers (eg, lysozyme and angiotensin-converting enzyme [ACE]) are lacking in high

65 These MPs exhibited angiotensin-converting enzyme activity and upregulated A

66 in downstream signaling pathways that induce angiotensin-converting enzyme expression and endothelial

67 elevation and 20-HETE-mediated increases in angiotensin-converting enzyme expression, endothelial dy

68 e activity and upregulated AT1 receptors and angiotensin-converting enzyme in P1 ECs.

69 duced residual albuminuria during fixed dose angiotensin-converting enzyme inhibition.

70 ptor blockers losartan and valsartan and the angiotensin-converting enzyme inhibitor captopril on wou

71 ejection fraction (HFrEF), compared with the angiotensin-converting enzyme inhibitor enalapril, and i

72 -angiotensin-aldosterone pathway, such as an angiotensin-converting enzyme inhibitor or an angiotensi

73 (<140 mm Hg systolic, <90 mm Hg diastolic), angiotensin-converting enzyme inhibitor or angiotensin r

74 It is an angiotensin-converting enzyme inhibitor that operates vi

75 ia could identify patients with COPD in whom angiotensin-converting enzyme inhibitor therapy improves

76 resent findings support the possibility that angiotensin-converting enzyme inhibitor treatment might

77 445-patient subset received at least 1 GDMT (angiotensin-converting enzyme inhibitor/angiotensin rece

78 The association between angiotensin-converting enzyme inhibitors (ACEI) and angi

79 re with reduced ejection fraction, including angiotensin-converting enzyme inhibitors (ACEI), angiote

80 Angiotensin-converting enzyme inhibitors (ACEIs) may ret

81 rm use of calcium channel blockers (CCBs) or angiotensin-converting enzyme inhibitors (ACEis), respec

82 ondition for which the medication was taken (angiotensin-converting enzyme inhibitors [ACEIs], angiot

83 ssessed for each of 6 drug classes: statins, angiotensin-converting enzyme inhibitors and angiotensin

84 were receiving insulin, and 84% were taking angiotensin-converting enzyme inhibitors or angiotensin

85 sting), prescribing appropriate medications (angiotensin-converting enzyme inhibitors or angiotensin-

86 m, as evidenced by trials that have compared angiotensin-converting enzyme inhibitors with drugs that

87 No class of medications (i.e., angiotensin-converting enzyme inhibitors, angiotensin-re

88 ives (eOC), hormonal replacement therapy, or angiotensin-converting enzyme inhibitors.

89 ficial effects of treatment with statins and angiotensin-converting enzyme inhibitors/angiotensin rec

90 , and 66.4% of the patients were on statins, angiotensin-converting enzyme inhibitors/angiotensin rec

91 es were treatment at discharge with statins, angiotensin-converting enzyme inhibitors/angiotensin rec

92 versus 57% in rural; P=0.1) and reversed for angiotensin-converting enzyme inhibitors/angiotensin rec

93 and 0.86 (0.74-1.01) in patients on statins, angiotensin-converting enzyme inhibitors/angiotensin rec

94 at it is also associated with a reduction of angiotensin-converting enzyme type 2 (ACE2) and an incre

95 vels of albumin excretion might benefit from angiotensin-converting-enzyme (ACE) inhibitors and stati

96 ha-amylase and alpha-glucosidase inhibition, angiotensin-converting-enzyme (ACE)-inhibition, antioxid

97 GET, 25 127 patients known to be tolerant to angiotensin-converting-enzyme (ACE)-inhibitors were rand

98 in Receptor-Neprilysin Inhibitor] With ACEI [Angiotensin-Converting-Enzyme Inhibitor] to Determine Im

99 ential introduction of medications including angiotensin-converting-enzyme inhibitors, angiotensin-re

100 io (10-fold enhancement) in the detection of angiotensin I is demonstrated using the DRILL interface

101 he HDX rates for a small 10-residue peptide, angiotensin I, in aqueous droplets, from which we found

102 es, majority of them were found identical to angiotensin I-converting enzyme (ACE) inhibitors, antiox

103 The angiotensin I-converting enzyme (ACE) inhibitory activit

104 showed different amino acid compositions and angiotensin I-converting enzyme (ACE) inhibitory potenti

105 ffect on proteolysis and negatively affected angiotensin I-converting enzyme inhibitory activity of f

106 acids), bioactivity (antioxidant effect and angiotensin I-converting enzyme inhibitory activity), rh

107 Angiotensin-I converting enzyme (ACE) is a zinc metallop

108 Activation of AT1 R with angiotensin II (30 nm) also increased TRPM4 currents in

109 K mutation in mice subjected to high salt or angiotensin II (Ang II) as models of hypertension and in

110 oconstrictor and a proinflammatory mediator, angiotensin II (Ang II) is considered a potential link b

111 um influx, and we have previously shown that angiotensin II (Ang II) via canonical transient receptor

112 We show that angiotensin II (Ang II), a vasoconstrictor, stimulates d

113 ing pathways involved in the effect of LC on angiotensin II (Ang II)-induced NADPH oxidase activation

114 E knockout (ApoE-KO) mice were infused with angiotensin II (AngII) for 28 days to induce AAA formati

115 ocytes and tubular epithelia and metabolizes angiotensin II (AngII), a peptide known to promote glome

116 Our studies have highlighted angiotensin II (AngII), a vasoactive hormone, as a poten

117 An Angiotensin II (AngII)-aldosterone (Ald) infusion mouse

118 Angiotensin II (applied for 2 h) reduced surface and tot

119 and hemodynamic responses to an infusion of angiotensin II (assessment of intrarenal renin-angiotens

120 Sodium deficiency increases angiotensin II (ATII) and aldosterone, which synergistic

121 ilar levels of hypertension after 2 weeks of angiotensin II administration.

122 Angiotensin II also reduced vasoconstriction stimulated

123 ctor (HIF)-1alpha and -2alpha in response to angiotensin II and hypoxia, respectively, which drive VE

124 where these tumor cells autocrinely produce angiotensin II by a chymase-dependent rather than an ang

125 critical role of hypoxia in producing local angiotensin II by a lactate-chymase-dependent mechanism

126 by subcutaneous infusion of either saline or Angiotensin II by osmotic minipumps.

127 included number of subjects, comorbidities, angiotensin II dose and duration, pressor effects, other

128 Angiotensin II effectively increased blood pressure in p

129 In WT mice, administration of angiotensin II for 2 weeks downregulated collectrin expr

130 sex chromosome complement were infused with angiotensin II for 28 days to induce AAAs.

131 We investigated the effectiveness of angiotensin II for the treatment of patients with this c

132 immune homeostasis independently of canonic angiotensin II generation.

133 nd point was reached by more patients in the angiotensin II group (114 of 163 patients, 69.9%) than i

134 ere reported in 60.7% of the patients in the angiotensin II group and in 67.1% in the placebo group.

135 occurred in 75 of 163 patients (46%) in the angiotensin II group and in 85 of 158 patients (54%) in

136 more severe dysfunction) was greater in the angiotensin II group than in the placebo group (-1.75 vs

137 s systematic review supports the notion that angiotensin II has an acceptable safety profile for use

138 was fatal in 55 of 115 patients treated with angiotensin II in case studies, cohort studies, and one

139 hanism and highlight the importance of local angiotensin II in regulating radioresistance of hypoxic

140 ension, and an impaired arterial response to angiotensin II in vivo.

141 Angiotensin II infusion in apoE(-/-) mice for 4 wk resul

142 Moreover, angiotensin II infusion instigated interferon-gamma, whi

143 n spontaneously hypertensive rat and chronic angiotensin II infusion rat models.

144 sporadic AAD induced by a high-fat diet and angiotensin II infusion, ADAMTS-4 deficiency (Adamts-4-/

145 testosterone as neonates or as adults before angiotensin II infusions.

146 dentified ACE2 as the main enzyme converting angiotensin II into angiotensin-(1-7) in human cerebrosp

147 We infused angiotensin II into endothelial-selective Epas1 knockout

148 Angiotensin II is an endogenous hormone with vasopressor

149 Moreover, although angiotensin II is the classic effector molecule of the R

150 Infusion of angiotensin II led to aortic medial hemorrhage and disse

151 The acute infusion of angiotensin II markedly increased the incidence of AAA i

152 protein-coupled receptor agonists, including angiotensin II or bombesin, induced rapid and persistent

153 Finally, we show that the enhanced angiotensin II plays an important role in the intracellu

154 Here, we find that the local angiotensin II predominantly exists in the hypoxic regio

155 damage, and suppression of cardio-reparative Angiotensin II receptor 2 (Agtr2).

156 the angiotensin II receptor, or losartan, an angiotensin II receptor blocker.

157 giotensin-converting enzyme (ACE) inhibitors/angiotensin II receptor blockers (ARB), beta-blockers an

158 Angiotensin II receptor blockers are beneficial in patie

159 We evaluated the impact of 3 generic angiotensin II receptor blockers commercialization on ad

160 sed case-control study indicates that use of angiotensin II receptor blockers might be associated wit

161 The effect of angiotensin II receptor blockers on right ventricular (R

162 reatitis and 61,637 controls, current use of angiotensin II receptor blockers was followed by a decre

163 titis, by degree of severity, among users of angiotensin II receptor blockers, as compared to non-use

164 angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers, beta-blockers, thiazid

165 cal research suggests a protective effect of angiotensin II receptor blockers.

166 d type, P = 7.8 x 10(-40)), which suppresses angiotensin II receptor signaling via allosteric transin

167 data analysis identified one important gene, angiotensin II receptor type 1 (AGTR1), in the Ca2+/AT-I

168 Substantial evidence indicates that the angiotensin II receptor type 1 (AT1 R) is inherently mec

169 027, a beta-arrestin-1-biased agonist of the angiotensin II receptor type 1 (AT1R), stimulates acute

170 it intracellular calcium release mediated by angiotensin II receptor type 1 (AT1R).

171 induced sympathoexcitation is independent of angiotensin II receptor type 1, oxytocin, ionotropic glu

172 cation of Telmisartan (an antagonist for the angiotensin II receptor) through copper-mediated C-H ami

173 0067, a beta-arrestin 2-biased ligand of the angiotensin II receptor, or losartan, an angiotensin II

174 nregulated collectrin expression in a type 1 angiotensin II receptor-dependent manner.

175 The angiotensin II receptors AT1R and AT2R serve as key comp

176 Activation of either AT1 Ra or AT1 Rb with angiotensin II stimulates TRPM4 currents in cerebral art

177 n of endothelium-dependent relaxation during angiotensin II stimulation.

178 nsors by allowing the short cationic peptide angiotensin II to be electrophoretically driven through

179 (AGT), angiotensin-converting enzyme (ACE), angiotensin II type 1 receptor (AGTR1), and aldosterone

180 The angiotensin II type 1 receptor (AT1R) is notable as it h

181 track activation and internalization of the angiotensin II type 1 receptor and the beta2 adrenocepto

182 aintained despite RVLM pretreatment with the angiotensin II type 1 receptor antagonist losartan, the

183 tics of graft injury in the presence of anti-angiotensin II type 1 receptor antibody (AT1R-Ab) and an

184 Agonistic angiotensin II type 1 receptor autoantibodies (AT1RaAbs)

185 VLM of normotensive rats is not mediated via angiotensin II type 1 receptor, oxytocin, ionotropic glu

186 occurs selectively on neurons, and neuronal angiotensin II type 1 receptors are indispensable to thi

187 Our data demonstrate that angiotensin II type 1 receptors promote ADAM17-mediated

188 system and ADAM17, we generated mice lacking angiotensin II type 1 receptors specifically on neurons.

189 Isolated de novo anti-angiotensin II type-1 receptor and anti-endothelin-1 typ

190 0 to 4 of 2009 with known HLA DSA status for angiotensin II type-1 receptor and endothelin-1 type A r

191 Adverse events associated with angiotensin II were infrequent; however, exacerbation of

192 other serious adverse events attributable to angiotensin II were reported.

193 Studies in which human subjects received IV angiotensin II were selected whether or not safety was d

194 activated in heart failure (norepinephrine, angiotensin II, aldosterone, and neprilysin) impair insu

195 received a study intervention (163 received angiotensin II, and 158 received placebo) and were inclu

196 ore age 60, blunted hypertensive response to angiotensin II, and a leftward shift in pressure natriur

197 o-HDL cholesterol ratio, C-reactive protein, angiotensin II, and albuminuria reduction and with incre

198 In mice challenged with angiotensin II, PDGF receptor alpha-positive cells were

199 echanistically, we found that Plk1 regulated angiotensin II-dependent activation of RhoA and actomyos

200 e protected against vascular remodelling and angiotensin II-dependent inflammation.

201 explore the repurposing of drugs that target angiotensin II-dependent NFkappaB signaling pathways to

202 ersus male (XY) sex chromosome complement on angiotensin II-induced AAA formation and rupture in phen

203 female mice exhibit far lower incidences of angiotensin II-induced AAAs than males.

204 eration-induced skeletal muscle fibrosis and angiotensin II-induced cardiac fibrosis.

205 Angiotensin II-induced hypertension was associated with

206 The angiotensin II-induced hypertension was attenuated by co

207 Although Angiotensin II-induced hypertension was blunted in PAI-1

208 The effect of the alphaAnalogue on angiotensin II-induced hypertension was investigated ove

209 In animal models of nitrate tolerance and angiotensin II-induced hypertension, decreased vasodilat

210 loid-specific Nox2 deletion had no effect on angiotensin II-induced hypertension, which, however, was

211 ox2, whereas endothelial cell Nox2 regulates angiotensin II-induced hypertension.

212 the hypoxia-inducible factor complex, during angiotensin II-induced hypertensive nephropathy provided

213 or signaling, in cultured fibroblasts and in angiotensin II-induced skin and heart fibrosis.

214 Angiotensin II-infused apoE(-/-) (n = 16) mice were used

215 Systemic delivery of anti-miR-181b in angiotensin II-infused Apoe(-/-) and Ldlr(-/-) mice atte

216 unappreciated roles for Micu2 in regulating angiotensin II-mediated hypertensive responses that are

217 treatment in hypertrophy samples, including angiotensin II-treated adult cardiac fibroblasts and ren

218 tration of small-molecule Plk1 inhibitors to angiotensin II-treated mice led to reduced arterial fitn

219 hancement, 100 picomole) in the detection of angiotensin II.

220 s is a systematic review of the safety of IV angiotensin II.

221 thout influencing the hypertensive effect of angiotensin II.

222 e subjected to pressure overload by means of angiotensin-II infusion or transversal aortic constricti

223 actors implicated in muscle atrophy, such as angiotensin-II, activin and Acvr2b, in SIRT6 depleted ce

224 rine analog (11)C-hydroxyephedrine), lack of angiotensin inhibition therapy, elevated B-type natriure

225 efits by selectively blocking the effects of angiotensin IV (AngIV) at its receptor (AT4R) with dival

226 Overall, our results implicate the angiotensin IV/AT4R cascade as a promising candidate for

227 range of the RAS was large, with equilibrium angiotensin levels being 8- to 10-fold higher compared w

228 to 10-fold higher compared with circulating angiotensin levels.

229 o)renin for conversion of Angiotensinogen to Angiotensin makes ATP6AP2 attractive for drug interventi

230 domains IV, V, VI, and VII had no effect on angiotensin-mediated beta-arrestin1 recruitment; however

231 nstrate that downregulation of Cygb prevents angiotensin-mediated hypertension.

232 Plasma angiotensin peptides represent a dynamic network that is

233 beta-arrestin2 recruitment to unliganded AT1 angiotensin receptor (AT1R).

234 ted, whereas acute HF and patients receiving angiotensin receptor blocker had higher plasma Ang II wi

235 been demonstrated that Valsartan (Val) as an angiotensin receptor blocker has renoprotective effects,

236 Combined angiotensin receptor blocker neprilysin inhibitors (ARNI

237 Angiotensin receptor blocker treatment may blunt the har

238 of associations and to explore the impact of angiotensin receptor blocker treatment.

239 nd to identify patients who can benefit from angiotensin receptor blocker treatment.

240 d angiotensin converting enzyme inhibitor or angiotensin receptor blocker usage were not significantl

241 , angiotensin-converting enzyme inhibitor or angiotensin receptor blocker use, and nonsmoking status-

242 DMT (angiotensin-converting enzyme inhibitor/angiotensin receptor blocker, or beta-blocker) at baseli

243 ngiotensin-converting enzyme inhibitor or an angiotensin receptor blocker, should generally be includ

244 c agent that combines a NEP inhibitor and an angiotensin receptor blocker.

245 for angiotensin-converting enzyme inhibitors/angiotensin receptor blockers (66% versus 68%; P=0.04) a

246 nsin-converting enzyme inhibitors (ACEI) and angiotensin receptor blockers (ARB) doses on outcomes in

247 otensin-converting enzyme inhibitors (ACEI), angiotensin receptor blockers (ARB), beta-blockers (BB),

248 The use of angiotensin receptor blockers (ARBs) correlates with red

249 iotensin converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs), beta blockers, and

250 tensin-converting enzyme inhibitors [ACEIs], angiotensin receptor blockers [ARBs], and beta-blockers

251 and angiotensin-converting enzyme inhibitors/angiotensin receptor blockers on outcome in patients wit

252 Chronic treatment with angiotensin receptor blockers was associated with better

253 ns, angiotensin-converting enzyme inhibitors/angiotensin receptor blockers, and beta-blockers, respec

254 ns, angiotensin-converting enzyme inhibitors/angiotensin receptor blockers, beta-blockers, and dual a

255 ns, angiotensin-converting enzyme inhibitors/angiotensin receptor blockers, beta-blockers, and dual a

256 angiotensin-converting enzyme inhibitors or angiotensin receptor blockers.

257 Sacubitril/valsartan, a combination angiotensin receptor-neprilysin inhibitor, improves morb

258 GM-HF trial (Prospective Comparison of ARNI [Angiotensin Receptor-Neprilysin Inhibitor] With ACEI [An

259 alocorticoid receptor antagonists (MRA), and angiotensin receptor-neprilysin inhibitors (ARNI), have

260 (angiotensin-converting enzyme inhibitors or angiotensin-receptor blockers and statins), and adverse

261 ng angiotensin-converting-enzyme inhibitors, angiotensin-receptor blockers, beta-blockers, and minera

262 ., angiotensin-converting enzyme inhibitors, angiotensin-receptor blockers, calcium channel blockers,

263 tural basis of the distinct functions of the angiotensin receptors, and may guide the design of new s

264 s, they reveal that a distinct population of angiotensin-sensitive neurons is integral to the coordin

265 The interaction between angiotensin signaling and NTS(HSD2) neurons provides a n

266 Knockout of the angiotensin subtype 2 receptors abolished the beneficial

267 e 1 receptor blockers, suggesting a role for angiotensin subtype 2 receptors in chronic wound healing

268 The renin-angiotensin system (RAS) and angiotensin AT1 receptors w

269 rsistent proteinuria despite optimised renin-angiotensin system (RAS) blockade.

270 Inappropriate activation of the renin-angiotensin system (RAS) exacerbates renal and vascular

271 The renin-angiotensin system (RAS) is a principal determinant of a

272 The renin-angiotensin system (RAS) is activated in heart failure (

273 Hypertension caused by increased renin-angiotensin system activation is associated with elevate

274 reactive oxygen species sources during renin-angiotensin system activation, with different Nox isofor

275 r assess the interaction between brain renin-angiotensin system and ADAM17, we generated mice lacking

276 itors with drugs that inhibit both the renin-angiotensin system and neprilysin.

277 ual inhibitors that interfere with the renin-angiotensin system at multiple sites have not yielded co

278 care alone, mostly involving optimized renin-angiotensin system blockade, which might generate furthe

279 ations between treatment with statins, renin-angiotensin system blockers, beta-blockers, dual antipla

280 In recent years, the renin-angiotensin system has emerged as a key mediator of stre

281 terious aspects of "stress." While the renin-angiotensin system has received some attention in this r

282 benefits produced by inhibitors of the renin-angiotensin system in heart failure has been modest, pos

283 both tissues and downregulation of the renin-angiotensin system in the kidney and mitogen-activated p

284 minuria, similar to that observed with renin-angiotensin system inhibition (losartan plus enalapril).

285 de complementary beneficial effects to renin-angiotensin system inhibition to slow progression of DN.

286 diabetic nephropathy on chronic stable renin-angiotensin system inhibitor treatment.

287 Thus, TGF-beta1 mAb added to renin-angiotensin system inhibitors did not slow progression o

288 could help to broaden the benefits of renin-angiotensin system inhibitors for patients with heart fa

289 llular environment without confounding renin-angiotensin system interactions.

290 Dysregulation of the skin renin-angiotensin system is implicated in abnormal wound heali

291 e that pharmacological blockade of the renin-angiotensin system may be considered for primary AF prev

292 lesterol, brain glucose, and the brain renin-angiotensin system, all of which are affected in some ne

293 survival effects of inhibitors of the renin-angiotensin system, as evidenced by trials that have com

294 After stimulation of the renin-angiotensin system, juxtaglomerular cells contained rhom

295 n-1d enzyme in a local juxtaglomerular renin-angiotensin system.

296 The presence of antibodies to angiotensin type 1 receptor (AT1R) and endothelin type A

297 the effects of topical reformulations of the angiotensin type 1 receptor blockers losartan and valsar

298 eceptors abolished the beneficial effects of angiotensin type 1 receptor blockers, suggesting a role

299 o structurally and functionally characterize angiotensin type-1a receptor-containing neurons of the p

300 se neuroanatomical techniques to reveal that angiotensin type-1a receptors are localized predominantl

301 While targeting endothelin and angiotensin, which are upstream regulators that promote