ライフサイエンスコーパス: renin-angiotensin system

1 lance between the classic and vasoprotective renin angiotensin system.

2 (V-ATPase) that may also function within the renin-angiotensin system.

3 ne or in combination with antagonists of the renin-angiotensin system.

4 ortant for regulating blood pressure via the renin-angiotensin system.

5 including inflammation, thrombosis, and the renin-angiotensin system.

6 malized by pharmacological inhibition of the renin-angiotensin system.

7 N-gamma-induced activation of the intrarenal renin-angiotensin system.

8 zyme-2 (ACE2) is a negative regulator of the renin-angiotensin system.

9 It is hypothesized to be a new member of the renin-angiotensin system.

10 y uncharacterized feedback loop in the local renin-angiotensin system.

11 he pro(renin) receptor and activation of the renin-angiotensin system.

12 ovel understanding of pathophysiology of the renin-angiotensin system.

13 l injury at least in part by suppressing the renin-angiotensin system.

14 early administration of drugs that block the renin-angiotensin system.

15 lete and thus more effective blockade of the renin-angiotensin system.

16 to have opposing physiological roles to the renin-angiotensin system.

17 ed pharmacologic approach to blockade of the renin-angiotensin system.

18 er systems controlled by ACE2, including the renin-angiotensin system.

19 n to counteract the effects of the classical renin-angiotensin system.

20 e renin-1d enzyme in a local juxtaglomerular renin-angiotensin system.

21 ulated through both the central and systemic renin-angiotensin systems.

22 rate-limiting step in the activation of the renin-angiotensin system, a key modulator of body fluid

23 Following stimulation of the renin-angiotensin system, A20 suppresses DC activation a

24 howed that a mouse model (ACE8/8) of cardiac renin-angiotensin system activation has a high rate of s

25 Renin-angiotensin system activation is a feature of many

26 Renin-angiotensin system activation is associated with a

27 Renin-angiotensin system activation is associated with c

28 Hypertension caused by increased renin-angiotensin system activation is associated with e

29 ffects that are preserved in the presence of renin-angiotensin system activation or heart failure.

30 n-13 infusions in the presence or absence of renin-angiotensin system activation with sodium depletio

31 rtant reactive oxygen species sources during renin-angiotensin system activation, with different Nox

32 in disease states characterized by enhanced renin-angiotensin system activation.

33 rotect against tissue injury associated with renin-angiotensin system activation.

34 mic risk in cardiac diseases associated with renin-angiotensin system activation.

35 e effective antiarrhythmic drugs in cases of renin-angiotensin system activation.

36 ing prolonged (Pyr(1))apelin-13 infusion and renin-angiotensin system activation.

37 iet modified F1 neonatal and adult offspring renin-angiotensin system activity and cardiovascular fun

38 ), we demonstrated that, on enhanced cardiac renin-angiotensin system activity, Cav1 dissociated from

39 fects on paternal cardiovascular function or renin-angiotensin system activity.

40 en cholesterol, brain glucose, and the brain renin-angiotensin system, all of which are affected in s

41 In recent years the renin-angiotensin system, already of recognised importan

42 lso studied the consequential effects on the renin angiotensin system and blood pressure.

43 that vitamin D deficiency activates both the renin angiotensin system and macrophage ER stress to con

44 further assess the interaction between brain renin-angiotensin system and ADAM17, we generated mice l

45 e key members of the alternative axis of the renin-angiotensin system and are expressed in HSPCs.

46 RGS5 signaling is linked to the renin-angiotensin system and directly controls vascular

47 The renin-angiotensin system and especially the angiotensin

48 ACE2 is a regulatory enzyme of the renin-angiotensin system and has protective functions in

49 Insulin stimulates the renin-angiotensin system and induces renal vasodilation.

50 Collectrin is an orphan member of the renin-angiotensin system and is a homolog of angiotensin

51 Because VDR ablation activates the renin-angiotensin system and leads to accumulation of an

52 inhibitors with drugs that inhibit both the renin-angiotensin system and neprilysin.

53 t activation and fibrosis in response to the renin-angiotensin system and post-MI remodeling.

54 e to classic signaling pathways, such as the renin-angiotensin system and sympathetic nervous system.

55 further evidence implicating the intrarenal renin-angiotensin system and take us one step further by

56 hereby suggesting that targeting of both the renin-angiotensin system and the EP1 receptor could be b

57 expression of the hAGT, up-regulation of the renin angiotensin system, and increased blood pressure a

58 rplay of the components of the non-canonical renin-angiotensin system, and discuss the function and t

59 diabetes associated with stimulation of the renin-angiotensin system, and further studies to assess

60 salt and fluid reabsorption, antagonizes the renin-angiotensin system, and inhibits oxidative stress.

61 ition to blood pressure, in part through the renin-angiotensin system, and insulin and glucose metabo

62 between the two key enzymes of the pulmonary renin-angiotensin system, angiotensin-converting enzyme,

63 Members of the renin-angiotensin system-angiotensin-converting enzymes

64 ne >/=160 mumol/l; hemoglobin </=120 g/l; no renin-angiotensin system antagonist; and no beta-blocker

65 Renin-angiotensin system antagonists help to control pro

66 Patients received beta-blockers, renin-angiotensin system antagonists, and statins withou

67 ated that this effect may be specific to the renin-angiotensin system as it did not replicate for bet

68 ce the survival effects of inhibitors of the renin-angiotensin system, as evidenced by trials that ha

69 e of dual inhibitors that interfere with the renin-angiotensin system at multiple sites have not yiel

70 ngiotensin system that regulates the classic renin angiotensin system axis.

71 inning this hypertension is an overactivated renin angiotensin system because ACE inhibition reverses

72 s not the result of enhanced activity of the renin-angiotensin system because circulating renin conce

73 edication, and a greater proportion received renin angiotensin system blockade (RASB) compared with i

74 (Renin-Angiotensin System Blockade Benefits in Clinical E

75 The RASTAVI (Renin-Angiotensin System Blockade Benefits in Clinical E

76 dition of aliskiren to standard therapy with renin-angiotensin system blockade in patients with type

77 tion suggest a possible therapeutic role for renin-angiotensin system blockade in reducing heart fail

78 Available data on the role of renin-angiotensin system blockade in renal transplantati

79 hieve statistical significance in benefit of renin-angiotensin system blockade on their primary combi

80 All the patients were treated with renin-angiotensin system blockade that had been adjusted

81 beneficial Ang 1-7/Mas axis concurrent with renin-angiotensin system blockade therapies inhibiting t

82 Renin-angiotensin system blockade therapy is associated

83 progressed to ESRD, the other seven received renin-angiotensin system blockade, and one also received

84 iduals with autosomal recessive disease with renin-angiotensin system blockade, possibly even before

85 rtive care alone, mostly involving optimized renin-angiotensin system blockade, which might generate

86 er min per 1.73 m(2), treated with optimized renin-angiotensin system blockade.

87 complimentary pharmacology and more complete renin-angiotensin system blockade.

88 ffect is amplified when BP is controlled via renin-angiotensin system blockade.

89 y disease and type 2 diabetes with optimized renin-angiotensin system blockade.

90 ine [g], >300 to 5000) and were treated with renin-angiotensin system blockade.

91 perglycaemic drugs, insulin, or both, plus a renin-angiotensin system blocker and an additional antih

92 with diabetes and hypertension, combining a renin-angiotensin system blocker with amlodipine, compar

93 on) trial compared the outcomes effects of a renin-angiotensin system blocker, benazepril, combined w

94 I, 0.72-0.76]; P < .001), and those who used renin-angiotensin system blockers (OR, 0.24 [95% CI, 0.0

95 Conclusions BB and renin-angiotensin system blockers alone or in combinatio

96 Results of previous studies suggest that renin-angiotensin system blockers might reduce the burde

97 ntihypertensive therapy that did not include renin-angiotensin system blockers was administered to ac

98 associations between treatment with statins, renin-angiotensin system blockers, beta-blockers, dual a

99 l stiffness, such as exercise and the use of renin-angiotensin system blockers, may be protective aga

100 3-6 months of optimized supportive care with renin-angiotensin system blockers.

101 pertensive regimens without beta-blockers or renin-angiotensin system blocking agents.

102 ed by hyperinsulinemia and activation of the renin-angiotensin system, both of which are associated w

103 ific deletion of Atp6ap2 does not affect the renin-angiotensin system but causes a combination of ren

104 Inhibition of the renin-angiotensin system by amniotic fluid stem cells ma

105 al Agt gene expression and activation of the renin-angiotensin system, by which hyperglycemia induces

106 The expression of renin-angiotensin system components was determined at 15

107 cardiovascular function by regulating other renin-angiotensin system components.

108 modulated in part by local activation of the renin-angiotensin system, compound the hyperglycemia-ind

109 This non-canonical axis of the renin-angiotensin system consists of angiotensin 1-7, an

110 Although the renin-angiotensin system contributes to fibrogenesis and

111 It is well known that the renin-angiotensin system contributes to left ventricular

112 rease in the vasoprotective axis of the lung renin-angiotensin system, decreased inflammatory cytokin

113 n prescribing (lipid-lowering, antiplatelet, renin-angiotensin system drugs).

114 alcium channel blocker, and a blocker of the renin- angiotensin system, either an ACE (angiotensin-co

115 7) are endogenous negative regulators of the renin-angiotensin system exerting cardioprotective effec

116 Pharmacological interruption of the renin-angiotensin system focuses on optimization of bloc

117 ng AngII, working in tandem with the central renin-angiotensin system, further exacerbates sympatho-h

118 n, a combination of genotype variants of the renin-angiotensin system genes is a powerful determinant

119 New evidence suggests that the brain renin angiotensin system has two opposing pathways: a da

120 This counter-regulatory renin-angiotensin system has a central role in the patho

121 The renin-angiotensin system has been implicated in posttrau

122 Inhibition of the renin-angiotensin system has been suggested to decrease

123 In recent years, the renin-angiotensin system has emerged as a key mediator o

124 n deleterious aspects of "stress." While the renin-angiotensin system has received some attention in

125 nsin-(1-9), a component of the non-canonical renin-angiotensin system, has a short half-life in blood

126 egies to target this important member of the renin-angiotensin system holds potential for the develop

127 f vitamin D receptor (VDR) and activation of renin angiotensin system; however, the involved mechanis

128 might help explain the relation between the renin-angiotensin system, hypertension, and Alzheimer's

129 Loss of ACE2 disrupts the balance of the renin-angiotensin system in a diabetic state and leads t

130 absorption through reciprocal effects on the renin-angiotensin system in a way that facilitates salt

131 Activation of the endogenous renin-angiotensin system in Cyp1a1Ren2 transgenic rats r

132 ation of renin release and activation of the renin-angiotensin system in health and disease.

133 nical benefits produced by inhibitors of the renin-angiotensin system in heart failure has been modes

134 Early blockade of the renin-angiotensin system in patients with type 1 diabete

135 ssion of periodontitis might involve a local renin-angiotensin system in periodontal tissue.

136 d the therapeutic potential of targeting the renin-angiotensin system in posttraumatic stress disorde

137 The recognition of the role the renin-angiotensin system in promoting insulin resistance

138 Modifying the renin-angiotensin system in sepsis should be further eva

139 e in vivo effects of CNIs on the local renal renin-angiotensin system in the collecting duct (CD).

140 hm in both tissues and downregulation of the renin-angiotensin system in the kidney and mitogen-activ

141 Although the role of the renin-angiotensin system in the pathophysiology of hyper

142 ta suggest that glucose can activate a local renin-angiotensin system in the podocyte, leading to inc

143 provides evidence supporting a role for the renin-angiotensin system in the regulation of the stress

144 opment of hypertension, thus implicating the renin-angiotensin system in this process.

145 Activation of the endogenous renin-angiotensin system in transgenic Cyp1a1Ren2 rats r

146 e evidence of involvement of nociception and renin-angiotensin systems in this effect.

147 increase in c-Src activity may help mediate renin-angiotensin system-induced arrhythmias and that c-

148 Renin-angiotensin system-induced Cav1 S-nitrosation was

149 n albuminuria, similar to that observed with renin-angiotensin system inhibition (losartan plus enala

150 o had received maximum labelled or tolerated renin-angiotensin system inhibition for at least 4 weeks

151 provide complementary beneficial effects to renin-angiotensin system inhibition to slow progression

152 target of the vascular protective action of renin-angiotensin system inhibition.

153 tested, including maximal inhibition of the renin-angiotensin system, inhibition of renal intracellu

154 IEW: Angioedema is a serious complication of renin-angiotensin system inhibitor therapy.

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

156 ive more often triple therapy (beta-blocker, renin-angiotensin system inhibitor, and mineralocorticoi

157 iuretics (94.2% versus 78.6%) and less often renin-angiotensin system inhibitors (75.4% versus 82.8%)

158 emains disputable about perioperative use of renin-angiotensin system inhibitors (RASi) and their out

159 Calcium channel blockers and renin-angiotensin system inhibitors are associated with

160 Prescription of renin-angiotensin system inhibitors at discharge was ass

161 Thus, TGF-beta1 mAb added to renin-angiotensin system inhibitors did not slow progres

162 tation could help to broaden the benefits of renin-angiotensin system inhibitors for patients with he

163 thesized that the benefits of treatment with renin-angiotensin system inhibitors in SARS-CoV-2 may ou

164 The prescribed dosages of beta-blockers and renin-angiotensin system inhibitors were significantly l

165 mostly but not entirely under treatment with renin-angiotensin system inhibitors.

166 ive cellular environment without confounding renin-angiotensin system interactions.

167 of activating the "alternative" axis of the renin-angiotensin system, involving ACE2, angiotensin-(1

168 Pharmacological inhibition of the renin-angiotensin system is a common approach to treat h

169 These observations demonstrate that the renin-angiotensin system is a key mediator of lung fibro

170 Overactivity of the brain renin-angiotensin system is a major contributor to neuro

171 The renin-angiotensin system is an important component of th

172 icate and extend prior observations that the renin-angiotensin system is associated with PTSD.

173 The central role of the renin-angiotensin system is discussed.

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

175 Blockade of the renin-angiotensin system is renoprotective in a variety

176 in-kinin system, along with the interlocking renin-angiotensin system, is a key regulator of vascular

177 (ACE), one of the central components of the renin-angiotensin system, is a key therapeutic target fo

178 After stimulation of the renin-angiotensin system, juxtaglomerular cells containe

179 ndicate that pharmacological blockade of the renin-angiotensin system may be considered for primary A

180 Long-term alterations of the brain renin-angiotensin system may influence signaling pathway

181 tensin II (AngII), the major effector of the renin-angiotensin system, mediates kidney disease progre

182 We measured levels of renin-angiotensin system messenger RNA and proteins in s

183 Insulin-induced activation of the renin-angiotensin system modulates insulin-induced renal

184 gies in terms of dosing and effectiveness of renin-angiotensin system-modulating agents for treatment

185 Treatment with inhibitors of the renin-angiotensin system often decreases the rate of pro

186 Experimental studies implicate the renin-angiotensin system, particularly angiotensin II ty

187 Recently, an alternative renin-angiotensin system pathway has been described, whi

188 Alzheimer's disease pathophysiology and the renin angiotensin system pathways suggest that angiotens

189 Chronic activation of the renin-angiotensin system plays a deleterious role in pro

190 The renin-angiotensin system plays an important role in the

191 host factors, such as the activation of the renin-angiotensin system, promote the progression of occ

192 ngiotensin II, the principal effector of the renin-angiotensin system, promotes vasoconstriction by a

193 ulting in acute lung inflammatory edema; the renin-angiotensin system, promoting cardiovascular insta

194 e hypothesize that the dynamic state of this renin-angiotensin system protective arm could influence

195 se, therapies that inhibit components of the renin angiotensin system (RAS) are also indicated, but t

196 Most physiologic effects of the renin angiotensin system (RAS) are mediated via the angi

197 The activation of the renin angiotensin system (RAS) has been implicated in th

198 The role of the renin angiotensin system (RAS) in atherosclerosis is com

199 Inappropriate activation of the renin angiotensin system (RAS) is a key contributor to t

200 Renin angiotensin system (RAS) is a key hormonal system

201 7), Mas receptor (ACE2/Ang-1-7/MasR), of the renin angiotensin system (RAS) is a potential therapeuti

202 Activation of the intrarenal renin angiotensin system (RAS) is believed to play an im

203 While blockade of the renin angiotensin system (RAS) is beneficial in treating

204 The Renin Angiotensin System (RAS), a key regulator of blood

205 ation of both the systemic and intra-tubular renin angiotensin systems (RAS), which are in turn assoc

206 The renin-angiotensin system (RAS) and angiotensin AT1 recep

207 d the relationship between the virus and the renin-angiotensin system (RAS) and how this might be aff

208 e of antihypertensive peptides acting on the renin-angiotensin system (RAS) and the endothelin (ET) s

209 ought association of genetic variants in the renin-angiotensin system (RAS) and vitamin D system with

210 ac outpatient clinic for the up-titration of renin-angiotensin system (RAS) antagonists and beta-bloc

211 A functioning placental renin-angiotensin system (RAS) appears necessary for unc

212 Components of the renin-angiotensin system (RAS) are expressed in a number

213 Physicians have embraced the concept of dual renin-angiotensin system (RAS) blockade hoping that it w

214 clinical studies have shown the benefits of renin-angiotensin system (RAS) blockade in the developme

215 Renin-angiotensin system (RAS) blockade reduces mortalit

216 Data are lacking on the effect of renin-angiotensin system (RAS) blockade therapy with ang

217 ), which reduces albuminuria, in addition to renin-angiotensin system (RAS) blockade, can slow progre

218 ps of baseline eGFR, albuminuria, and use of renin-angiotensin system (RAS) blockade.

219 and persistent proteinuria despite optimised renin-angiotensin system (RAS) blockade.

220 It has been speculated that renin-angiotensin system (RAS) blockers may promote COVI

221 Activation of the intrarenal renin-angiotensin system (RAS) can elicit hypertension i

222 Inappropriate activation of the renin-angiotensin system (RAS) contributes to many CKDs.

223 Furthermore, ACE and the renin-angiotensin system (RAS) directly regulate hemangi

224 Inappropriate activation of the renin-angiotensin system (RAS) exacerbates renal and vas

225 An altered renin-angiotensin system (RAS) has been implicated as a

226 The renin-angiotensin system (RAS) has emerged as a key path

227 The renin-angiotensin system (RAS) has long been appreciated

228 Medications aimed at inhibiting the renin-angiotensin system (RAS) have been used extensivel

229 The increased activity of intrarenal renin-angiotensin system (RAS) in a setting of elevated

230 ests that inflammation and activation of the renin-angiotensin system (RAS) increases sympathetic dri

231 It is unknown whether stopping renin-angiotensin system (RAS) inhibitor therapy in pati

232 Intervention with aspirin, atorvastatin or renin-angiotensin system (RAS) inhibitors effectively at

233 udy was to explore the potential benefits of renin-angiotensin system (RAS) inhibitors on left ventri

234 ephropathy already receiving stable doses of renin-angiotensin system (RAS) inhibitors.

235 The renin-angiotensin system (RAS) is a key regulator of the

236 The renin-angiotensin system (RAS) is a major physiological

237 The renin-angiotensin system (RAS) is a principal determinan

238 The renin-angiotensin system (RAS) is activated in heart fai

239 The renin-angiotensin system (RAS) is an important regulator

240 Pathological activation of the renin-angiotensin system (RAS) is associated with the me

241 The circulating, endocrine renin-angiotensin system (RAS) is important to circulato

242 The renin-angiotensin system (RAS) mediates proapoptotic, pr

243 paB activation, endothelium dysfunction, and renin-angiotensin system (RAS) over-activity in thoracic

244 The products of the renin-angiotensin system (RAS) play an important role in

245 The renin-angiotensin system (RAS) plays a critical role in

246 The renin-angiotensin system (RAS) plays a major role in liv

247 The renin-angiotensin system (RAS) plays an important role i

248 The renin-angiotensin system (RAS) plays pathogenic roles in

249 The renin-angiotensin system (RAS) regulates blood pressure

250 The renin-angiotensin system (RAS) regulates BP and may affe

251 re underlying pathophysiology related to the renin-angiotensin system (RAS) that may be clinically in

252 renewed interest in therapies targeting the renin-angiotensin system (RAS) to improve beta-cell func

253 Kallikrein activity was inhibited while the renin-angiotensin system (RAS) upregulated in the kidney

254 mpus is associated with gene variants of the renin-angiotensin system (RAS), a system implicated in v

255 The active hormone of the renin-angiotensin system (RAS), angiotensin II (Ang II),

256 zyme 2 (ACE2) is a negative regulator of the renin-angiotensin system (RAS), catalyzing the conversio

257 iac mast cells (MC), thus activating a local renin-angiotensin system (RAS), culminating in ventricul

258 Here, we propose that the renin-angiotensin system (RAS), in addition to its centr

259 At comparable BP control, inhibitors of the renin-angiotensin system (RAS), including angiotensin co

260 etermined by the coordinated activity of the renin-angiotensin system (RAS), including the balanced s

261 eceptor (PRR), a key regulator of intrarenal renin-angiotensin system (RAS), is predominantly present

262 ced glomerular filtration, activation of the renin-angiotensin system (RAS), oxidative/nitrative stre

263 onic kidney disease and up-regulation of the renin-angiotensin system (RAS), which is deleterious to

264 diabetes mellitus includes activation of the renin-angiotensin system (RAS), which may lead to hypert

265 types 1 and 2 and ACE2 are components of the renin-angiotensin system (RAS).

266 evidence for a regulatory role in the human renin-angiotensin system (RAS).

267 3 deficiency in mice (DPP3(-/-)) affects the renin-angiotensin system (RAS).

268 on from cardiac mast cells activates a local renin-angiotensin system (RAS).

269 and argue that this is due to a dysregulated renin-angiotensin system (RAS).

270 are frequently associated with an activated renin-angiotensin-system (RAS) and increased levels of i

271 bitors or angiotensin receptor blockers (ie, renin-angiotensin system [RAS] antagonists) did not reac

272 and provide evidence that inhibition of the renin-angiotensin system reduces glomerulosclerosis in a

273 Notably, 10-week inhibition of the renin-angiotensin system regenerated kidney vasculature

274 differential expression of multiple central renin-angiotensin system regulators in adult offspring k

275 tion of sodium-glucose transporter-2 and the renin-angiotensin system, remains a concern.

276 Activation of the renin angiotensin system resulting in stimulation of ang

277 , which do not counteract any longer the CPC renin-angiotensin system, resulting in cellular senescen

278 TGF-beta1 and renin-angiotensin system signaling alters the fibroblast

279 Antihypertensive medications that target the renin angiotensin system, such as angiotensin receptor b

280 ave suggested that medications targeting the renin-angiotensin system, such as angiotensin-converting

281 factor-like ligand 1A and components of the renin-angiotensin system, support the importance of IL-1

282 ary enzyme of the vasoprotective axis of the renin angiotensin system that regulates the classic reni

283 dogenous 7-amino acid peptide hormone of the renin-angiotensin system that has antiproliferative prop

284 s, is involved in both Wnt signaling and the renin-angiotensin system that regulates blood pressure.

285 that activation of the protective arm of the renin angiotensin system, the angiotensin-converting enz

286 ceptor and the impact this action has on the renin-angiotensin system, the body's innate immune respo

287 ng enzyme 2 has expanded from regulating the renin angiotensin system to regulating intestinal amino

288 hypertensive agents that did not inhibit the renin-angiotensin system to reach targets of under 135 m

289 The contribution of the intrarenal renin-angiotensin system to the development of hypertens

290 sults demonstrate the existence of an airway renin-angiotensin system triggered by release of mast-ce

291 Exposure to agents acting on the renin-angiotensin system was not associated with a risk

292 portive care (in particular, blockade of the renin-angiotensin system) was adjusted on the basis of p

293 capable of restraining overactivation of the renin-angiotensin system, which contributes to exuberant

294 ssociated with an imbalance of the pulmonary renin-angiotensin system, which correlates with aggravat

295 LS diet induces the activation of the renin-angiotensin system, which increases oxidative stre

296 nds upon stimulation of AS expression by the renin-angiotensin system, which takes 12 h to reach full

297 sted the hypothesis that interruption of the renin-angiotensin system with either an angiotensin-conv

298 suggests that activation of the alternative renin-angiotensin system with the nonpeptide Mas recepto

299 [Ang-(1-7)] is an endogenous peptide of the renin-angiotensin system with vasodilator and antiprolif

300 In the central renin-angiotensin system, zinc-dependent aminopeptidase