ライフサイエンスコーパス: angiotensin

1 flammatory angiotensin (Ang) II peptide into angiotensin 1-7 (Ang 1-7), a peptide which opposes the a

2 ates angiotensin receptor types 1 and 2, and angiotensin 1-7 and alamandine, which activate MAS proto

3 ngiotensin-converting enzyme 2) and Ang 1-7 (angiotensin 1-7) are endogenous negative regulators of t

4 of the renin-angiotensin system consists of angiotensin 1-7, angiotensin 1-9, angiotensin-converting

5 iotensin system consists of angiotensin 1-7, angiotensin 1-9, angiotensin-converting enzyme 2, the ty

6 ogy of ARDS, whereas activation of the ACE-2-angiotensin(1-7)-angiotensin AT(2) receptor and the ACE-

7 -7)-angiotensin AT(2) receptor and the ACE-2-angiotensin(1-7)-Mas receptor pathways have been shown t

8 n and is degraded by ACE and enhanced by the angiotensin(1-9) produced by ACE2.

9 A controlled release of angiotensin-(1-9) is needed for its delivery to the hear

10 R laser irradiation, a controlled release of angiotensin-(1-9) was achieved from the LipoTherm-AuNC n

11 Angiotensin-(1-9), a component of the non-canonical reni

12 im was to develop a drug delivery system for angiotensin-(1-9).

13 HF were similar, regardless of LVEF or renin-angiotensin-aldosterone inhibitor use.

14 The renin-angiotensin-aldosterone level was suppressed during pool

15 coronavirus-2 that interfaces with the renin-angiotensin-aldosterone system (RAAS) through angiotensi

16 ron is adjusted with activation of the renin-angiotensin-aldosterone system (RAAS).

17 rting enzyme, which is a member of the renin-angiotensin-aldosterone system (RAAS).

18 s shows that increased activity of the renin-angiotensin-aldosterone system contributes to increased

19 related to medications that act on the renin-angiotensin-aldosterone system in patients exposed to co

20 ic obstructive pulmonary disease, BMI, renin-angiotensin-aldosterone system inhibitor use, and other

21 ta-blockers, n = 20; and withdrawal of renin-angiotensin-aldosterone system inhibitors and beta-block

22 Renin-angiotensin-aldosterone system inhibitors and risk of Co

23 jects were randomized to withdrawal of renin-angiotensin-aldosterone system inhibitors and/or beta-bl

24 blocker therapy, n = 20; withdrawal of renin-angiotensin-aldosterone system inhibitors, n = 20; withd

25 nt women partly through the suppressed renin-angiotensin-aldosterone system.

26 racial differences in activity of the renin-angiotensin-aldosterone system.

27 t, to the conversion of the pro-inflammatory angiotensin (Ang) II peptide into angiotensin 1-7 (Ang 1

28 art failure, combined beta-blocker and renin-angiotensin antagonist medication rates increased from 6

29 giotensin converting enzyme-1-angiotensin II-angiotensin AT(1) receptor pathway contributes to the pa

30 eas activation of the ACE-2-angiotensin(1-7)-angiotensin AT(2) receptor and the ACE-2-angiotensin(1-7

31 lin is an important contributor to the renin-angiotensin axis, regulating cardiovascular, metabolic,

32 e AT2 cells express the SARS-CoV-2 receptors angiotensin converting enzyme (ACE2) and transmembrane p

33 protein to bind to the cell surface receptor angiotensin converting enzyme 2 (ACE2) glycoprotein and

34 Angiotensin converting enzyme 2 (ACE2) plays an importan

35 and block spike protein interaction with the angiotensin converting enzyme 2 (ACE2) with 1-5 nM affin

36 is brief perspective, we examine the role of angiotensin converting enzyme 2 as the receptor for seve

37 The role of angiotensin converting enzyme 2 has expanded from regula

38 Recently, angiotensin converting enzyme 2 was identified as a prim

39 soluble forms of the receptor for the virus, angiotensin converting enzyme 2.

40 The angiotensin converting enzyme-1-angiotensin II-angiotens

41 hophysiology has been proposed: imbalance of angiotensin converting enzymes (ACE)1 and ACE2 (ACE2 bei

42 ycation end products (AGEs), the activity of angiotensin-converting (ACE) and acetylcholinesterase (A

43 ignificant changes in serum, lung and kidney angiotensin-converting enzyme (ACE) activity, establishe

44 Angiotensin-converting enzyme (ACE) affects blood pressu

45 Angiotensin II, converted by angiotensin-converting enzyme (ACE) from angiotensin I a

46 The top three most common medications were angiotensin-converting enzyme (ACE) inhibitors (17.9%),

47 F) beyond conventional therapy consisting of angiotensin-converting enzyme (ACE) inhibitors or angiot

48 Targeted overexpression of angiotensin-converting enzyme (ACE), an amyloid-beta pro

49 fit heart, we measured the mRNA of renin and angiotensin-converting enzyme (ACE), and found both were

50 Angiotensin-converting enzyme 2 (ACE-2), neprilysin (NEP

51 main (RBD) showing crucial interactions with angiotensin-converting enzyme 2 (ACE2) and cross-reactin

52 ausing COVID-19, is facilitated by host cell angiotensin-converting enzyme 2 (ACE2) and transmembrane

53 s critical for SARS-CoV-2 infection, namely, angiotensin-converting enzyme 2 (ACE2) and transmembrane

54 SARS-CoV-2 and the human cellular receptor, angiotensin-converting enzyme 2 (ACE2) are both densely

55 SARS-CoV-2 uses human angiotensin-converting enzyme 2 (ACE2) as its receptor t

56 Early evidence pointed to angiotensin-converting enzyme 2 (ACE2) as SARS-CoV-2 ent

57 how that S2E12 and S2M11 competitively block angiotensin-converting enzyme 2 (ACE2) attachment and th

58 ity RNA in situ mapping revealed the highest angiotensin-converting enzyme 2 (ACE2) expression in the

59 coronaviruses to utilize animal orthologs of angiotensin-converting enzyme 2 (ACE2) for cell entry.

60 This study compares angiotensin-converting enzyme 2 (ACE2) gene expression,

61 Angiotensin-converting enzyme 2 (ACE2) has been identifi

62 locked S conformation, resulting in reduced angiotensin-converting enzyme 2 (ACE2) interaction in vi

63 Angiotensin-converting enzyme 2 (ACE2) is an entry recep

64 SARS-CoV-2 spike protein binding to angiotensin-converting enzyme 2 (ACE2) is critical for v

65 Although angiotensin-converting enzyme 2 (ACE2) is crucial for SA

66 In particular, activity of the angiotensin-converting enzyme 2 (ACE2) is dysregulated i

67 Angiotensin-converting enzyme 2 (ACE2) is the canonical

68 ry syndrome coronavirus 2 (SARS-CoV-2) binds angiotensin-converting enzyme 2 (ACE2) on host cells to

69 RBD) of the spike protein binds to the human angiotensin-converting enzyme 2 (ACE2) receptor as a pre

70 SARS-CoV-2 spike protein and blocking to the Angiotensin-converting enzyme 2 (ACE2) receptor in a sin

71 were engineered to stably express the human angiotensin-converting enzyme 2 (ACE2) receptor, but sta

72 action of receptor binding domain (RBD) with angiotensin-converting enzyme 2 (ACE2) receptor.

73 use of species-specific differences in their angiotensin-converting enzyme 2 (ACE2) receptors.

74 racts with both cellular heparan sulfate and angiotensin-converting enzyme 2 (ACE2) through its recep

75 Infection of human angiotensin-converting enzyme 2 (ACE2) transgenic mice a

76 SARS-CoV-2 spike (S) protein binds angiotensin-converting enzyme 2 (ACE2), and in concert w

77 - SARS-CoV-2 - gains entry to host cells via angiotensin-converting enzyme 2 (ACE2), highlighting the

78 onavirus 2 (SARS-CoV-2) viral association to angiotensin-converting enzyme 2 (ACE2), its main host re

79 in is a candidate vaccine antigen that binds angiotensin-converting enzyme 2 (ACE2), leading to virus

80 The receptor for SARS-CoV-2 binding, angiotensin-converting enzyme 2 (ACE2), was not detected

81 r-binding domain (RBD) and its host receptor angiotensin-converting enzyme 2 (ACE2), which regulate b

82 SARS-CoV spike protein and its host receptor angiotensin-converting enzyme 2 (ACE2), which regulate b

83 lar localization of the SARS-CoV-2 receptor, angiotensin-converting enzyme 2 (ACE2), within the upper

84 V-2 and SARS-CoV recognize the same receptor-angiotensin-converting enzyme 2 (ACE2)-in humans(3,4).

85 izes an epitope that partially overlaps with angiotensin-converting enzyme 2 (ACE2)-interacting sites

86 protein (S(RBD)) from interacting with human angiotensin-converting enzyme 2 (ACE2).

87 19 (Covid-19), because the viral receptor is angiotensin-converting enzyme 2 (ACE2).

88 ost cell infection is mediated by binding to angiotensin-converting enzyme 2 (ACE2).

89 ted coronavirus (SARS-CoV-2) that uses human angiotensin-converting enzyme 2 (hACE2) as the entry rec

90 In response to human receptor angiotensin-converting enzyme 2 (hACE2), S opens sequent

91 domain (RBD) are compared with those between angiotensin-converting enzyme 2 and RBD complexes.

92 han SARS-CoV according to computed S protein-angiotensin-converting enzyme 2 binding free energy chan

93 r by adsorptive transcytosis and that murine angiotensin-converting enzyme 2 is involved in brain and

94 oV-2 spike glycoprotein (S protein) and host angiotensin-converting enzyme 2 receptor following mutat

95 f its spike protein S1 to attach to the host angiotensin-converting enzyme 2 receptor in lung and air

96 ronavirus 2, which invades cells through the angiotensin-converting enzyme 2 receptor.

97 2 (SARS-CoV-2) and mice expressing the human angiotensin-converting enzyme 2 receptor.

98 Although angiotensin-converting enzyme 2 serves as the portal for

99 Human angiotensin-converting enzyme 2(ACE2) was identified as

100 ACE2 (angiotensin-converting enzyme 2) and Ang 1-7 (angiotensi

101 ACE2 (angiotensin-converting enzyme 2) and NEP (neprilysin) in

102 2 infection is binding of the virus to ACE2 (angiotensin-converting enzyme 2) on the airway epitheliu

103 ACE2 (angiotensin-converting enzyme 2), and TMPRSS2 (transmemb

104 CoV-2 to invade endothelial cells via ACE-2 (angiotensin-converting enzyme 2), which is expressed on

105 ose receptor binding domain (RBD) recognizes angiotensin-converting enzyme 2, initiating conformation

106 inent effects on host proteins, most notably angiotensin-converting enzyme 2, might also provide wort

107 ally, NETs triggered by SARS-CoV-2 depend on angiotensin-converting enzyme 2, serine protease, virus

108 onsists of angiotensin 1-7, angiotensin 1-9, angiotensin-converting enzyme 2, the type 2 angiotensin

109 ke protein trimer immunoglobulin G inhibited angiotensin-converting enzyme 2-spike protein binding to

110 ion of the functional receptor of the virus, angiotensin-converting enzyme 2.

111 red by binding of the viral spike protein to angiotensin-converting enzyme 2.

112 ngiotensin-aldosterone system (RAAS) through angiotensin-converting enzyme 2.

113 a to inhibit the binding of spike protein to angiotensin-converting enzyme 2.

114 hin its trimeric spike glycoprotein to human angiotensin-converting enzyme 2.

115 s in F2 neonatal offspring growth and tissue angiotensin-converting enzyme activity were programmed b

116 bitor (lisinopril) and thus was dependent on angiotensin-converting enzyme catalytic activity.

117 rotein binding to the human receptor protein angiotensin-converting enzyme II (ACE2).

118 conflicting regarding whether chronic use of angiotensin-converting enzyme inhibitor (ACEI) or angiot

119 neficial ACE10 phenotype was reversed by the angiotensin-converting enzyme inhibitor (lisinopril) and

120 ent with a glomerular disease with either an angiotensin-converting enzyme inhibitor or an angiotensi

121 rular status, birth weight, premature birth, angiotensin-converting enzyme inhibitor use, angiotensin

122 geting the renin-angiotensin system, such as angiotensin-converting enzyme inhibitors (ACE-Is) and an

123 vestigated continued and discontinued use of angiotensin-converting enzyme inhibitors (ACEi) or angio

124 e first mechanistic evidence that the use of angiotensin-converting enzyme inhibitors (ACEI) or angio

125 The role of angiotensin-converting enzyme inhibitors (ACEIs) and ang

126 It has been hypothesized that angiotensin-converting enzyme inhibitors (ACEIs)/angiote

127 ere -4.38 mm Hg (95% CI, -7.27 to -2.16) for angiotensin-converting enzyme inhibitors and -3.07 mm Hg

128 prescribed drugs in the same year, including angiotensin-converting enzyme inhibitors and angiotensin

129 On admission, medical therapy, including angiotensin-converting enzyme inhibitors and angiotensin

130 view that found high-certainty evidence that angiotensin-converting enzyme inhibitors and angiotensin

131 Patients receiving beta-blockers or angiotensin-converting enzyme inhibitors had a higher ri

132 clinical evidence does not support stopping angiotensin-converting enzyme inhibitors or angiotensin

133 ves as the portal for infection, the role of angiotensin-converting enzyme inhibitors or angiotensin

134 syndrome coronavirus 2 (SARS-CoV-2) receptor angiotensin-converting enzyme receptor type-2 (ACE2) and

135 um testing within 30 days of initiating ACE (angiotensin-converting enzyme) inhibitor or angiotensin

136 used to inhibit the activity of neprilysin, angiotensin-converting enzyme, or aminopeptidase N, resp

137 One such effector was angiotensin-converting enzyme, which is a member of the

138 ssion of the SARS-CoV-2 viral entry receptor angiotensin-converting enzyme-2 (ACE2).

139 the first evidence for therapeutic roles of angiotensin-converting enzyme-overexpressing macrophages

140 ly inhibition of dipeptidyl peptidase IV and angiotensin-converting enzyme.

141 Members of the renin-angiotensin system-angiotensin-converting enzymes (ACEs) ACE and ACE2, angi

142 used regarding a potential harmful effect of angiotensin-converting-enzyme (ACE) inhibitors and angio

143 of angiotensin-receptor blockers (ARBs) and angiotensin-converting-enzyme (ACE) inhibitors and the r

144 shown to produce beneficial effects on renin-angiotensin-dependent rodent models and human hypertensi

145 ence suggests that the metabolic products of angiotensin I and II - initially thought to be biologica

146 by angiotensin-converting enzyme (ACE) from angiotensin I and metabolized by ACE 2 (ACE2), plays a p

147 Several variants were shown to block angiotensin I cleavage in vitro, highlighting their pote

148 encoded residues dominate recognition of the angiotensin I converting enzyme 2 (ACE2)-binding site.

149 by blocking the ACE-dependent conversion of angiotensin I to the potent vasoconstrictor angiotensin

150 tment of High-Output Shock) trial for renin, angiotensin I, and angiotensin II concentrations before

151 The peptide inhibition of the angiotensin I-converting enzyme (ACE) from its default b

152 valuate transgenic mice expressing the human angiotensin I-converting enzyme 2 (ACE2) receptor driven

153 gain insights into its interactions with the angiotensin I-converting enzyme 2 (ACE2)-solute carrier

154 Previously, we have shown that loss of angiotensin-I converting enzyme 2 (ACE2) promotes the AC

155 hey protein hydrolysates (WPHs) obtained had angiotensin-I-converting enzyme (ACE) and dipeptidyl pep

156 Angiotensin II (Ang II) stimulation induced trafficking

157 nsin-converting enzymes (ACEs) ACE and ACE2, angiotensin II (Ang II), Ang-(1-7), and receptors AT1 an

158 rbate vascular senescence and progression of angiotensin II (Ang II)-induced AAA by facilitating reac

159 eceptor") that results in tissue injury from angiotensin II (Ang II)-mediated signaling.

160 as profiles: the balanced endogenous agonist angiotensin II (AngII) and two strongly beta-arrestin-bi

161 ding partners and that activation of AT1R by angiotensin II (ANGII) elicits beta-arrestin-dependent i

162 We present evidence that following angiotensin II (AngII) infusion the TNFalpha type 1 rece

163 Inhibition of angiotensin II (AngII) signaling, a therapeutic mainstay

164 switching to a similar extent as TGFbeta1 or angiotensin II (ANGII) stimulation.

165 merulosa (ZG) under the control of the renin-angiotensin II (AngII) system.

166 e upregulated during hypertension induced by angiotensin II (AngII).

167 Furthermore, the cellular responses to angiotensin II and the relative abundance of fibrogenic

168 nction in rats, and the impact of intrarenal angiotensin II AT(1) receptor blockade using candesartan

169 These results suggest that blockade of angiotensin II AT(1) receptors has a major impact upon o

170 s reversed by an ACE inhibitor but not by an angiotensin II AT1 receptor antagonist.

171 Angiotensin II caused a significant increase in mean art

172 t Shock) trial for renin, angiotensin I, and angiotensin II concentrations before the start of admini

173 Here we demonstrate that within the rosette, angiotensin II evokes periodic Ca(v)3-dependent calcium

174 mples from patients enrolled in the ATHOS-3 (Angiotensin II for the Treatment of High-Output Shock) t

175 Our data reveal a critical role for angiotensin II in regulating burst occurrence, and a mul

176 hermore, telemetry studies showed that while angiotensin II increased blood pressure acutely in all a

177 Rationale: Exogenous angiotensin II increases mean arterial pressure in patie

178 Following angiotensin II infusion in mice, we found that an affini

179 ion or chronic neurohormonal stimulation via Angiotensin II infusion.

180 ations before the start of administration of angiotensin II or placebo and after 3 hours.Measurements

181 angiotensin-converting enzyme 2, the type 2 angiotensin II receptor (AT(2)R), the proto-oncogene Mas

182 51 matched pairs initiating ACE inhibitor or angiotensin II receptor blocker therapy between January

183 (angiotensin-converting enzyme) inhibitor or angiotensin II receptor blocker therapy.

184 ensin-converting enzyme inhibitors (ACEi) or angiotensin II receptor blockers (ARB) during hospitaliz

185 ensin-converting enzyme inhibitors (ACEI) or angiotensin II receptor blockers (ARBs) does not increas

186 Because angiotensin II receptor blockers, ACE inhibitors, and mi

187 e collected from patients, with attention to angiotensin II receptor blockers, such as olmesartan, al

188 -2 binding, ACE2 downregulation enhances the angiotensin II receptor type 1 (AT(1) R) axis associated

189 n, and LOX-1 has been shown to interact with angiotensin II receptor type 1 (AT1).

190 Exogenous angiotensin II reduced catecholamine vasopressor doses a

191 Thus, STBEVs reduced angiotensin II responsiveness in normal pregnancy, but n

192 e ACE2, leading to toxic overaccumulation of angiotensin II that induces acute respiratory distress s

193 2 cleaves many biological substrates besides angiotensin II to control vasodilatation and vascular pe

194 s and shifts in cellular communication after angiotensin II treatment that promote the development of

195 this work, we present crystal structures of angiotensin II type 1 receptor (AT1R) (2.7 to 2.9 angstr

196 le nanobodies that act as antagonists of the angiotensin II type 1 receptor (AT1R).

197 rrestin bias and G protein bias arise at the angiotensin II type 1 receptor.

198 Angiotensin II type-1 receptor (AT1R) antibodies have be

199 angiotensin I to the potent vasoconstrictor angiotensin II while simultaneously halting the NEP-depe

200 ress, and hypertrophy and attenuates Ang II (angiotensin II) and deoxycorticosterone acetate-salt ind

201 The levels of ET-1(endothelin-1) and Ang II (Angiotensin II) in the plasma were measured by an enzyme

202 perivascular tissues in response to Ang II (angiotensin II)-mediated hypertension, miR-214 showed th

203 to myofibroblasts in the presence of Ang II (angiotensin II).

204 e to 2 weeks of continuous administration of angiotensin II, a profibrotic stimulus that drives patho

205 these adaptive responses; reduces levels of angiotensin II, aldosterone, and ET-1; reduces ammoniage

206 activity repressed by albumin, high glucose, angiotensin II, aldosterone, cisplatin and lipopolysacch

207 In euvolemic rats, the dipsogenic hormone angiotensin II, but not the orexigenic hormone ghrelin,

208 Angiotensin II, converted by angiotensin-converting enzy

209 myocyte pathological hypertrophy induced by Angiotensin II, phenylephrine, and isoproterenol, but di

210 ation events by altering the balance between angiotensin II, which activates angiotensin receptor typ

211 The angiotensin converting enzyme-1-angiotensin II-angiotensin AT(1) receptor pathway contri

212 a multifaceted therapeutic effect to prevent angiotensin II-induced cardiac dysfunction by improving

213 Oxidized LDL (a LOX-1 ligand) increased angiotensin II-induced vasoconstriction in STBEV-incubat

214 blood pressure independent of alterations in angiotensin II-mediated aortic stiffness.

215 itro findings were confirmed in vivo with an angiotensin II-mediated murine model of cardiac fibrosis

216 ce with a combination of a high-fat diet and angiotensin II.

217 ility to remodel cardiac tissue and generate angiotensin II.

218 synthesis of its main effector peptides Ang (angiotensin) II and Ang (1-7).

219 This study tests a direct role of IgE in angiotensin-II (Ang-II) perfusion- and peri-aortic CaCl(

220 converting enzyme 2 (ACE2) promotes the ACE/angiotensin-II (Ang-II)/angiotensin type 1 receptor (AT1

221 The angiotensin-II antagonist losartan is a promising candid

222 Chronic infusion of angiotensin-II in atheroprone (ApoE(-/-)) mice provides

223 ], Rho guanine nucleotide exchange factor 6, angiotensin-II type 1 receptor, endothelin type A recept

224 nificantly improved extraction of a range of angiotensins known to possess important roles in blood p

225 The metabolic changes and altered angiotensin levels observed in male DPP3(-/-) mice were

226 Circulating and equilibrium angiotensin peptide levels strongly correlated in our pa

227 circulating and equilibrium levels of plasma angiotensin peptide profiles were assessed using novel l

228 ays using the purified enzyme confirmed that angiotensin peptides are substrates for DPP3.

229 However, angiotensin peptides can also bind to receptors differen

230 d water homeostasis by degrading circulating angiotensin peptides.

231 egradation inhibition through neprilysin and angiotensin receptor blockade, has led to groundbreaking

232 tensin-converting enzyme inhibitor (ACEI) or angiotensin receptor blocker (ARB) influences disease ou

233 comparable antihypertensive activity to the angiotensin receptor blocker (ARB) losartan.

234 Providing the anti-fibrotic angiotensin receptor blocker losartan to mice in drinkin

235 angiotensin-converting enzyme inhibitor use, angiotensin receptor blocker use, BMI z-score for age an

236 sin Receptor-Neprilysin Inhibitor] with ARB [Angiotensin Receptor Blocker] Global Outcomes in HFpEF),

237 Pre-hospital use vs. non-use of angiotensin receptor blockers (aOR 2.02, CI 1.03-3.96) a

238 tensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs) and beta blockers.

239 has revealed that ACE inhibitors (ACEIs) or angiotensin receptor blockers (ARBs) may be beneficial i

240 otensin-converting enzyme inhibitors (ACEIs)/angiotensin receptor blockers (ARBs) may make patients m

241 in-converting enzyme inhibitors (ACE-Is) and angiotensin receptor blockers (ARBs), may be associated

242 angiotensin-converting enzyme inhibitors or angiotensin receptor blockers in patients with COVID-19.

243 angiotensin-converting enzyme inhibitors or angiotensin receptor blockers requires further investiga

244 angiotensin-converting enzyme inhibitors and angiotensin receptor blockers use, was similar between c

245 angiotensin-converting enzyme inhibitors and angiotensin receptor blockers.

246 and -3.07 mm Hg (95% CI, -4.99 to -1.44) for angiotensin receptor blockers.

247 derlies increased placental HIF-1alpha in an angiotensin receptor type 1 receptor agonistic autoantib

248 eptors different from AT(1)R, in particular, angiotensin receptor type II (AT(2)R), resulting in biol

249 ACE2 together with angiotensin receptor types 1 and 2 and ACE2 are componen

250 ance between angiotensin II, which activates angiotensin receptor types 1 and 2, and angiotensin 1-7

251 PARAGON-HF (Prospective Comparison of ARNI [Angiotensin Receptor-Neprilysin Inhibitor] with ARB [Ang

252 neralocorticoid receptor antagonists [MRAs], angiotensin receptor-neprilysin inhibitors [ARNIs], and

253 scle fibrosis and improved pain Losartan, an angiotensin-receptor blocker with anti-fibrotic abilitie

254 A potential association between the use of angiotensin-receptor blockers (ARBs) and angiotensin-con

255 sin-converting enzyme inhibitors (ACEIs) and angiotensin-receptor blockers (ARBs) in coronavirus dise

256 ensin-converting-enzyme (ACE) inhibitors and angiotensin-receptor blockers (ARBs) in this clinical co

257 angiotensin-converting enzyme inhibitors and angiotensin-receptor blockers are not associated with gr

258 ween previous treatment with ACE inhibitors, angiotensin-receptor blockers, beta-blockers, calcium-ch

259 ssociated with increased activation of brain angiotensin receptors, enhanced sympathetic nervous syst

260 relationship between the virus and the renin-angiotensin system (RAS) and how this might be affected

261 It has been speculated that renin-angiotensin system (RAS) blockers may promote COVID-19 b

262 The renin-angiotensin system (RAS) has long been appreciated as a

263 hat inflammation and activation of the renin-angiotensin system (RAS) increases sympathetic drive.

264 It is unknown whether stopping renin-angiotensin system (RAS) inhibitor therapy in patients w

265 krein activity was inhibited while the renin-angiotensin system (RAS) upregulated in the kidney of KS

266 ned by the coordinated activity of the renin-angiotensin system (RAS), including the balanced synthes

267 r (PRR), a key regulator of intrarenal renin-angiotensin system (RAS), is predominantly presented in

268 1 and 2 and ACE2 are components of the renin-angiotensin system (RAS).

269 ciency in mice (DPP3(-/-)) affects the renin-angiotensin system (RAS).

270 dified F1 neonatal and adult offspring renin-angiotensin system activity and cardiovascular function

271 on paternal cardiovascular function or renin-angiotensin system activity.

272 Renin-angiotensin system antagonists help to control proteinur

273 hat this effect may be specific to the renin-angiotensin system as it did not replicate for beta-bloc

274 (Renin-Angiotensin System Blockade Benefits in Clinical Evoluti

275 The RASTAVI (Renin-Angiotensin System Blockade Benefits in Clinical Evoluti

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

277 icial Ang 1-7/Mas axis concurrent with renin-angiotensin system blockade therapies inhibiting the det

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

279 This non-canonical axis of the renin-angiotensin system consists of angiotensin 1-7, angioten

280 endogenous negative regulators of the renin-angiotensin system exerting cardioprotective effects in

281 This counter-regulatory renin-angiotensin system has a central role in the pathogenesi

282 cs (94.2% versus 78.6%) and less often renin-angiotensin system inhibitors (75.4% versus 82.8%) compa

283 Prescription of renin-angiotensin system inhibitors at discharge was associate

284 ed that the benefits of treatment with renin-angiotensin system inhibitors in SARS-CoV-2 may outweigh

285 The renin-angiotensin system is an important component of the card

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

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

288 thesize that the dynamic state of this renin-angiotensin system protective arm could influence long-t

289 involved in both Wnt signaling and the renin-angiotensin system that regulates blood pressure.

290 yme 2 has expanded from regulating the renin angiotensin system to regulating intestinal amino acid h

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

292 1-9), a component of the non-canonical renin-angiotensin system, has a short half-life in blood.

293 f sodium-glucose transporter-2 and the renin-angiotensin system, remains a concern.

294 ggested that medications targeting the renin-angiotensin system, such as angiotensin-converting enzym

295 Members of the renin-angiotensin system-angiotensin-converting enzymes (ACEs)

296 ounteract the effects of the classical renin-angiotensin system.

297 E2) promotes the ACE/angiotensin-II (Ang-II)/angiotensin type 1 receptor (AT1R) axis, a deleterious a

298 ngiotensin-converting enzyme inhibitor or an angiotensin type 1 receptor blocker.

299 The present study highlights a role for angiotensin Type 1a receptor expressing neurons located

300 Although it is clear that central angiotensin type 1a receptors (AT1aR; encoded by the Agt