ライフサイエンスコーパス: aldosterone

1 lthough the MR is present in fish, they lack aldosterone.

2 nes, including the mineralocorticoid hormone aldosterone.

3 ssociated with strong stimulation of PRA and aldosterone.

4 were injected with lipopolysaccharide and/or aldosterone.

5 extracellular water, eGFR, plasma renin, and aldosterone.

6 l canine RV and LV to cyclic overstretch and aldosterone.

7 rate-limiting enzyme in the biosynthesis of aldosterone.

8 ndependent of the increased plasma levels of aldosterone.

9 Aldosterone (10(-9) to 10(-7) M) increased Akt/mTOR/Rapt

10 ty, -1.27 vs. 0.81 ng/mL/h, p = 0.002; serum aldosterone, -180.9 vs. 3.1 ng/mL/h, p = 0.03), resultin

11 ut (IL-1R(-/-)) mice treated with vehicle or aldosterone (600 microg.kg(-1).d(-1) for 14 days through

12 alysis, and in vitro studies determined that aldosterone activates EGFR-dependent signaling.

13 Aldosterone activates the intercalated cell mineralocort

14 Aldosterone activation of AP-1 may contribute to its pro

15 Aldosterone acutely activates NCC to modulate renal NaCl

16 Aldosterone affects serum potassium and is associated wi

17 shown that long-term systemic treatment with aldosterone (ALD) can enhance NKCC1 protein expression a

18 An Angiotensin II (AngII)-aldosterone (Ald) infusion mouse model of hypertension w

19 Aldosterone (Aldo) promotes fibrosis in myocardium, and

20 and ENaC interactions might be modulated by aldosterone (Aldo).

21 rates, the MR mediates sodium homeostasis by aldosterone and also acts as a receptor for cortisol.

22 Plasma aldosterone and ascorbic acid concentrations are not ass

23 y produce the salt-retaining steroid hormone aldosterone and cause millions of cases of severe hypert

24 hypertension, whereas no association between aldosterone and hypertension was seen when renin was not

25 results from renin-independent production of aldosterone and is a common cause of hypertension.

26 l analyses investigated associations between aldosterone and MR activity, assessed via serum potassiu

27 role of inhibition of the renin-angiotensin-aldosterone and neprilysin pathways, as well as the limi

28 egulation results from the interplay between aldosterone and plasma potassium.

29 Atherosclerosis) with measurements of serum aldosterone and plasma renin activity (PRA).

30 ates pendrin, as well as the effect of serum aldosterone and potassium on this response, we measured

31 duced increased levels of corticosterone and aldosterone and showed a high proliferation index.

32 r other clinical outcomes based on cortisol, aldosterone, and ascorbic acid concentrations.

33 linical outcomes based on baseline cortisol, aldosterone, and ascorbic acid concentrations.Methods: F

34 I, 1.00-1.27; P = 0.04), but total cortisol, aldosterone, and ascorbic acid were not.Conclusions: In

35 paracrine hormones including angiotensin II, aldosterone, and endothelin-1 (ET-1) that mediate the im

36 responses; reduces levels of angiotensin II, aldosterone, and ET-1; reduces ammoniagenesis; and dimin

37 kedly raised plasma renin activity (PRA) and aldosterone, and exerted more effective anti-albuminuric

38 art failure (norepinephrine, angiotensin II, aldosterone, and neprilysin) impair insulin sensitivity

39 pokalemic hypertension, suppressed renin and aldosterone, and no mutations in the genes encoding beta

40 iuretic hormones, such as angiotensin II and aldosterone; and adipokines, particularly leptin.

41 ity was repressed by acetylcholine, albumin, aldosterone, angiotensin II, high glucose, cisplatin and

42 erved Cardiac Function Heart Failure With an Aldosterone Antagonist (TOPCAT) trial of 1372 patients w

43 (Aldosterone Antagonist Therapy for Adults With Heart Fai

44 ion >=45% from 3 large HFpEF trials (TOPCAT [Aldosterone Antagonist Therapy for Adults With Heart Fai

45 erved Cardiac Function Heart Failure with an Aldosterone Antagonist trial).

46 erved Cardiac Function Heart Failure With an Aldosterone Antagonist Trial).

47 erved Cardiac Function Heart Failure With an Aldosterone Antagonist Trial; n=218).

48 erved Cardiac Function Heart Failure With an Aldosterone Antagonist) trial participants (n = 379) usi

49 erved Cardiac Function Heart Failure With an Aldosterone Antagonist) was categorized as poor, interme

50 ed Cardiac Function in Heart Failure With an Aldosterone Antagonist), 719 (19%) patients had AF on th

51 erved Cardiac Function Heart Failure with an Aldosterone Antagonist).

52 Spironolactone (SP), an FDA approved aldosterone antagonist, triggers the proteasomal degrada

53 nt with ACE inhibitor, ARB, beta blocker, or aldosterone antagonist.

54 erved Cardiac Function Heart Failure With an Aldosterone Antagonist; n=3445) comparing spironolactone

55 receptor blockers (ARBs), beta blockers, and aldosterone antagonists in adults with systemic RVs.

56 of ACE inhibitors, ARBs, beta blockers, and aldosterone antagonists in patients with systemic RVs.

57 Aldosterone antagonists slow the progression of chronic

58 s of treatment with ACE inhibitors, ARBs, or aldosterone antagonists, there was no statistically sign

59 sin) II blockers, neprilysin inhibitors, and aldosterone antagonists.

60 In addition, we evaluated aldosterone as a potential effect modifier of these asso

61 t was perhaps mandatory if the appearance of aldosterone as a specific mediator of the homeostatic sa

62 Plasma aldosterone, B-type natriuretic peptide, active renin co

63 inuria during single-agent renin-angiotensin-aldosterone blockade is accompanied by improved cardiore

64 ed by albumin, high glucose, angiotensin II, aldosterone, cisplatin and lipopolysaccharide.

65 Suppression of renin and higher aldosterone concentrations in the context of this renin

66 Higher aldosterone concentrations were associated with lower se

67 With renin suppression, higher aldosterone concentrations were independently associated

68 antihypertensive drugs, plasma potassium and aldosterone concentrations, and plasma renin concentrati

69 Longitudinal analyses investigated whether aldosterone concentrations, in the context of physiologi

70 L, 0.039 ng/uL, 0.43 ng/uL, 0.0076 ng/uL for aldosterone, corticosterone, cortisol, and beta-estrone,

71 On the basis of their measured activities, aldosterone, cortisol, 11-deoxycorticosterone, corticost

72 ed with older age, whereas serum and urinary aldosterone did not significantly decline.

73 Genetic alteration of ENaC-alpha causes aldosterone dysregulation in patients, highlighting that

74 feedback loop that contributes to a form of aldosterone escape in vivo.

75 Aldosterone excess is a pathogenic factor in many hypert

76 Aldosterone excess is common in patients with RHTN, and

77 Fluid retention, mediated largely by aldosterone excess, is the predominant mechanism underly

78 with hyperaldosteronism or normal levels of aldosterone exhibited increased activity of NLRP3 inflam

79 and e' velocity, respectively, whereas serum aldosterone explained 19% of the indirect effects betwee

80 P450 11B2 catalyzes aldosterone formation from 11-deoxycorticosterone throug

81 s changes in endocrine systems, including in aldosterone function and glycemic control.

82 milieu comprising minimum cortisol and high aldosterone, growth hormone (GH), and prolactin levels,

83 Among those with high-normal aldosterone (>/=9 ng/dL, n = 202), we found no significa

84 h serum hormone concentrations (cortisol and aldosterone), hepatobiliary enzyme levels, white blood c

85 In participants with normal aldosterone, high-normal serum potassium was associated

86 Aldosterone improved 5-day survival, invasive arterial p

87 revious work provides evidence for a role of aldosterone in alcohol use disorders (AUDs).

88 that hAS overexpression increased levels of aldosterone in hAS(+/-) mice.

89 ole enzyme responsible for the production of aldosterone in humans.

90 and found that women had larger increases in aldosterone in response to an angiotensin-II infusion th

91 But the acute effects of aldosterone in the DCT are less well understood.

92 and women with type 2 diabetes, implicating aldosterone in the pathophysiology of coronary microvasc

93 Both aging and inappropriate secretion of aldosterone increase the risk for developing cardiovascu

94 Plasma aldosterone increased briefly after high-dose PDE9-I in

95 In addition, aldosterone increased the expression of NLRP3, active ca

96 Aldosterone increases NaCl reabsorption via NCC over the

97 However, aldosterone-induced cardiac hypertrophy is totally preve

98 studies showed that macitentan decreased the aldosterone-induced cardiomyocyte hypertrophy.

99 fection with 11beta-HSD2 siRNA abolished the aldosterone-induced CTGF up-regulation.

100 A well characterized aldosterone-induced gene is the serum and glucocorticoid

101 Lipocalin 2 may be important in modulating aldosterone-induced inflammation, monocyte activation, a

102 Repression of MR and SGK1 by aldosterone-induced miRs may represent a negative feedba

103 NSC23766 prevented the aldosterone-induced proliferation and migration of cardi

104 involved in vesicular transport, as a novel aldosterone-induced protein that can alter Na(+) transpo

105 s showed that NLRP3 in immune cells mediates aldosterone-induced vascular damage.

106 uria with hypertension in uninephrectomized, aldosterone-infused, and high salt-fed (ALDO) systemic G

107 Mice underwent d-aldosterone infusion, uninephrectomy, and were given 1%

108 lar, regardless of LVEF or renin-angiotensin-aldosterone inhibitor use.

109 ertain medications such as renin angiotensin aldosterone inhibitors.

110 Notably, aldosterone interactions with both GR and MR demonstrate

111 With high circulating aldosterone, intercalated cell mineralocorticoid recepto

112 With high circulating aldosterone, intercalated cell mineralocorticoid recepto

113 Aldosterone is a major mineralocorticoid hormone that pl

114 ating NCC are unclear, but in animal models, aldosterone is a potent regulator, possibly via effects

115 Aldosterone is important for the regulation of electroly

116 The mineralocorticoid aldosterone is produced in the adrenal zona glomerulosa

117 We found that although aldosterone is produced processively, the enzyme prefere

118 rast, when dietary potassium intake is high, aldosterone is stimulated.

119 The corticosteroid aldosterone is the physiological activator of the MR in

120 ne, theophylline) and hormones (vasopressin, aldosterone) known to exacerbate cysts elicit NHA2 expre

121 The renin-angiotensin-aldosterone level was suppressed during pool walking: th

122 We therefore examined aldosterone levels and found that women had larger incre

123 Notably, the increase in aldosterone levels expected on NaCl depletion was attenu

124 Aldosterone levels positively correlated with the number

125 whereas blood pressure, renin activity, and aldosterone levels remained unchanged.

126 -abstinent patients had significantly higher aldosterone levels than abstinent patients.

127 ary aldosteronism was diagnosed when urinary aldosterone levels were higher than 12 mug/24 h.

128 decreases in plasma renin activity and serum aldosterone levels were more evident in pool walking tha

129 by further reducing cortisol and increasing aldosterone levels) and reduces T and B cell counts, lik

130 intron conversion have (a) increased plasma aldosterone levels, (b) increased hCYP11B2 mRNA and prot

131 In Study 3, the relationship between plasma aldosterone levels, alcohol drinking and craving was inv

132 investigated the relationship between plasma aldosterone levels, ethanol self-administration and the

133 K+ diet, despite a 10-fold increase in serum aldosterone levels, implying that mTORC2 regulates kaliu

134 receptor (MR) antagonists to reduce elevated aldosterone levels, which are associated with deleteriou

135 peutic interventions in conditions with high aldosterone levels.

136 d multivariable models, in those with normal aldosterone (<9 ng/dL, n = 1163), participants in the hi

137 this African-American cohort, we found that aldosterone may modify the association between serum pot

138 elationship between ethanol drinking and the aldosterone/MR pathway in three different species.

139 h pro-inflammatory cytokines with or without aldosterone, nuclear factor-kappaB inhibitor BAY 11-7082

140 echanisms leading to the damaging effects of aldosterone on the cardiovascular system.

141 effects of systolic blood pressure and serum aldosterone on the relationship between ESI and strain a

142 rican cohort, and to determine the effect of aldosterone on this association.

143 oral sodium suppression test, regardless of aldosterone or renin levels, as a confirmatory diagnosti

144 vs. OR, 1.16; 95% CI, 1.02-1.32; P = 0.75), aldosterone (OR, 1.01; 95% CI, 0.97-1.05 vs. OR, 1.01; 9

145 terone synthase (CYP11B2) is associated with aldosterone overproduction.

146 cant interaction between serum potassium and aldosterone (P = 0.046).

147 ation (P=0.01) and a trend for higher plasma aldosterone (P=0.06), but measures of home BP, plasma an

148 tic agent that acts on the renin-angiotensin-aldosterone pathway, such as an angiotensin-converting e

149 elated autonomous aldosteronism and abnormal aldosterone physiology that provides 1 potential explana

150 olved in the deleterious vascular effects of aldosterone, placing NLRP3 as a potential target for the

151 ntribute to increased cell proliferation and aldosterone producing adenoma (APA) development.

152 ry aldosteronism (PA) and its main subtypes, aldosterone-producing adenoma (APA) and bilateral adrena

153 y/beta-catenin signaling may be important in aldosterone-producing adenoma (APA).

154 Aldosterone-producing adenomas (APAs) are benign tumors

155 ype 1 and of CaV1.3-R3 (R990H) identified in aldosterone-producing adenomas conducts omega-currents i

156 In human aldosterone-producing adrenocortical cancer cell lines,

157 age (r=-0.431, P<0.0001), whereas the total aldosterone-producing cell cluster area was positively c

158 glomerulosa CYP11B2 expression and increased aldosterone-producing cell cluster expression.

159 The integrated ratio of aldosterone-producing cell cluster to CYP11B2-expressing

160 mal foci of CYP11B2-expressing cells, called aldosterone-producing cell clusters, were analyzed.

161 ntity (93%) to a closely related enzyme, the aldosterone-producing CYP11B2.

162 Aldosterone-producing zona glomerulosa (zG) cells of the

163 consistent with increased renin-independent aldosterone production and hypertension.

164 q signaling is sufficient for adrenocortical aldosterone production and implicate this pathway in the

165 Cyp11b2 transcription and aldosterone production are predominantly regulated by An

166 Mutations in different genes increase aldosterone production in PA, but additional mechanisms

167 onism is a nonsuppressible renin-independent aldosterone production that causes hypertension and card

168 s a prevalent continuum of renin-independent aldosterone production that parallels the severity of hy

169 in membrane depolarization, calcium influx, aldosterone production, and cell proliferation.

170 ategory had a continuum of renin-independent aldosterone production, where greater severity of produc

171 lated to tumorigenesis rather than excessive aldosterone production.

172 successful cannulation and lateralization of aldosterone production.

173 ncoding aldosterone synthase) expression and aldosterone production.

174 quantify the magnitude of renin-independent aldosterone production.

175 In vitro, aldosterone rapidly increased intracellular cAMP and ino

176 cription (OR, 0.70 [95% CI, 0.55-0.90]); and aldosterone receptor antagonist prescription (OR, 0.46 [

177 uring normal and low Na(+) conditions, while aldosterone receptors mainly affect oxygen metabolism fo

178 ts to induce or repress the transcription of aldosterone-regulated genes.

179 Aldosterone regulates electrolyte and fluid homeostasis

180 Aldosterone regulates pendrin through mechanisms both de

181 onpressor effects included changes in plasma aldosterone, renal function, cardiac variables, and elec

182 The aldosterone-renin ratio had poor sensitivity and negativ

183 tes of primary aldosteronism testing (plasma aldosterone-renin) and the association of testing with e

184 The greater aldosterone responsivity in women may be a mechanism for

185 tor ablation blunted, but did not eliminate, aldosterone's effect on pendrin total and apical abundan

186 R30, a membrane-associated receptor, limited aldosterone's effects on NCC activity ex vivo, and NCC p

187 disease; however, the influence of aging on aldosterone secretion and physiology is not well underst

188 Coupled with suppression of aldosterone secretion, activation of NCC helps to retain

189 illators to control zG layer performance and aldosterone secretion.

190 However, aberrant signaling in the aldosterone-sensitive distal nephron (ASDN) and inhibiti

191 quaporin 2-positive principal cells of mouse aldosterone-sensitive distal nephron where ENaC is local

192 multiple rat nephron segments, including the aldosterone-sensitive distal nephron where the epithelia

193 ransport in several epithelia, including the aldosterone-sensitive distal nephron, distal colon, and

194 annel in the thick ascending limb and in the aldosterone-sensitive distal nephron.

195 ory NTS, focusing on a medial subregion with aldosterone-sensitive HSD2 neurons.

196 e neurons in the subfornical organ (SFO) and aldosterone-sensitive neurons in the nucleus of the soli

197 Here we show that chemogenetic activation of aldosterone-sensitive neurons that express 11beta-hydrox

198 eceptor kinase) signaling, renin angiotensin aldosterone signaling and beta-2 adrenergic receptor sig

199 The final steps in the Renin-Angiotensin-Aldosterone signaling System (RAAS) involve binding of t

200 Aldosterone significantly increased after 6- and 12-mont

201 Aldosterone significantly increases NCC activity within

202 ths after randomization (n = 1,776) included aldosterone, soluble ST2 (sST2), tissue inhibitor of mat

203 At baseline, the profibrotic biomarkers aldosterone, sST2, TIMP-1, Gal-3, PINP, and PIIINP were

204 Eight months after randomization, aldosterone, sST2, TIMP-1, MMP-9, PINP, and PIIINP had d

205 Aldosterone-stimulated MR nuclear translocation was bloc

206 role of microRNAs (miRs) induced by extended aldosterone stimulation in regulating MR and SGK1 has no

207 R-466b and preventing its upregulation after aldosterone stimulation increased amiloride-sensitive so

208 R of mouse MR were profiled by qRT-PCR after aldosterone stimulation.

209 ensitive sodium transport and sensitivity to aldosterone stimulation.

210 Aldosterone synthase (AS, cytochrome P450 11B2, cyp11B2)

211 The relationship between age and adrenal aldosterone synthase (CYP11B2) expression was evaluated

212 Aldosterone synthase (CYP11B2) inhibitors have been expl

213 In PA, hypomethylation of aldosterone synthase (CYP11B2) is associated with aldost

214 angiotensin II type 1 receptor (AGTR1), and aldosterone synthase (CYP11B2), including sex-SNP or SNP

215 d by dysregulated localization of the enzyme aldosterone synthase (Cyp11b2), which is normally restri

216 the effects of increased expression of human aldosterone synthase (hAS) on blood pressure (BP), we es

217 d overexpression of P450 11B2 (also known as aldosterone synthase) can lead to hypertension, congesti

218 J5MUT-induced induction of CYP11B2 (encoding aldosterone synthase) expression and aldosterone product

219 Fadrozole (an inhibitor of aldosterone synthase) treatment significantly reduced BP

220 ochrome P450 side chain cleavage enzyme) and aldosterone synthase, it did inhibit 3betaHSD2 expressio

221 subfamily B member 2 (hCYP11B2) gene encodes aldosterone synthase, the rate-limiting enzyme in the bi

222 evolution of terrestrial vertebrates and of aldosterone synthesis.

223 diet was used to stimulate renin-angiotensin-aldosterone system (RAAS) activation, and serum lipocali

224 rdiovascular function: the renin-angiotensin-aldosterone system (RAAS) and the sympathetic nervous sy

225 Renin-angiotensin aldosterone system (RAAS) inhibitors significantly impro

226 2 that interfaces with the renin-angiotensin-aldosterone system (RAAS) through angiotensin-converting

227 g hormones involved in the renin-angiotensin-aldosterone system (RAAS).

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

229 ted with activation of the renin-angiotensin-aldosterone system (RAAS).

230 (assessment of intrarenal renin-angiotensin-aldosterone system [RAAS]) were measured before and afte

231 ion and RSNA contribute to renin-angiotensin-aldosterone system activation.

232 some content is altered by renin-angiotensin-aldosterone system activation.

233 ncluding inhibitors of the renin-angiotensin-aldosterone system and beta blockers) is useful only whe

234 olve interactions with the renin-angiotensin aldosterone system and Nox1/4.

235 d by interactions with the renin-angiotensin-aldosterone system and reactive oxygen species derived f

236 predominantly involve the renin-angiotensin-aldosterone system and the adrenal glucocorticoid pathwa

237 ological inhibition of the renin-angiotensin-aldosterone system as a therapeutic strategy is one of t

238 s, steroid minimization or renin-angiotensin-aldosterone system blockade result in better preservatio

239 increased activity of the renin-angiotensin-aldosterone system contributes to increased oxygen metab

240 significant interaction of renin-angiotensin-aldosterone system drugs with renin in this population.

241 fects on the dysfunctional renin-angiotensin-aldosterone system during vasoplegic shock.

242 SNPs at key renin-angiotensin-aldosterone system genes associate with systolic blood p

243 Renin-angiotensin-aldosterone system genes have been inconsistently associ

244 tire 6-h protocol, whereas renin-angiotensin-aldosterone system hormones were within the lower normal

245 irus-2) has implicated the renin-angiotensin-aldosterone system in acute respiratory distress syndrom

246 edications that act on the renin-angiotensin-aldosterone system in patients exposed to coronavirus di

247 th other inhibitors of the renin-angiotensin-aldosterone system in patients with HF.

248 th other inhibitors of the renin-angiotensin-aldosterone system increases the risk of hyperkalemia.

249 bitor group versus the non-renin-angiotensin-aldosterone system inhibitor group (10.7 vs 18.1 microg/

250 rsus 69.7 mm Hg in the non-renin-angiotensin-aldosterone system inhibitor group (p = 0.298).

251 ours was 72.2 mm Hg in the renin-angiotensin-aldosterone system inhibitor group versus 69.7 mm Hg in

252 y lower at 24 hours in the renin-angiotensin-aldosterone system inhibitor group versus the non-renin-

253 Renin-angiotensin-aldosterone system inhibitor patients had lower total co

254 24 hours compared with non-renin-angiotensin-aldosterone system inhibitor patients.

255 tients who were on chronic renin-angiotensin-aldosterone system inhibitor therapy as outpatients and

256 ts who were not on chronic renin-angiotensin-aldosterone system inhibitor therapy as outpatients.

257 causation bias as stopping renin angiotensin aldosterone system inhibitor therapy in the advent of hy

258 ressin who were on chronic renin-angiotensin-aldosterone system inhibitor therapy versus those receiv

259 ressin who were on chronic renin-angiotensin-aldosterone system inhibitor therapy with those who were

260 in who were not on chronic renin-angiotensin-aldosterone system inhibitor therapy.

261 ve pulmonary disease, BMI, renin-angiotensin-aldosterone system inhibitor use, and other potential co

262 (ACE2), but whether or not renin-angiotensin-aldosterone system inhibitors (RAASi) would be beneficia

263 n = 20; and withdrawal of renin-angiotensin-aldosterone system inhibitors and beta-blockers, n = 20)

264 Renin-angiotensin-aldosterone system inhibitors and risk of Covid-19.

265 andomized to withdrawal of renin-angiotensin-aldosterone system inhibitors and/or beta-blockers versu

266 erkalemia, especially when renin-angiotensin-aldosterone system inhibitors are used.

267 eta-blockers, statins, and renin-angiotensin-aldosterone system inhibitors) initiated after myocardia

268 apy, n = 20; withdrawal of renin-angiotensin-aldosterone system inhibitors, n = 20; withdrawal of bet

269 sociations between age and renin-angiotensin-aldosterone system physiology.

270 Abnormal activity of the renin-angiotensin-aldosterone system plays a causal role in the developmen

271 e of drugs that act on the renin-angiotensin-aldosterone system were recorded prospectively.

272 ment via modulation of the renin-angiotensin-aldosterone system with angiotensin receptor blockers or

273 Fallot: Inhibition of the Renin-Angiotensin-Aldosterone System) is an investigator-initiated, multic

274 ells and by regulating the renin-angiotensin-aldosterone system, adiposity, energy expenditure, and p

275 ncludes suppression of the renin-angiotensin-aldosterone system, pressure natriuresis, and reduced re

276 tide and kinin systems and renin-angiotensin-aldosterone system, respectively.

277 similar activation of the renin-angiotensin-aldosterone system, whereas only dKO mice displayed a lo

278 ol through blockade of the renin-angiotensin-aldosterone system.

279 tly through the suppressed renin-angiotensin-aldosterone system.

280 e as key components of the renin-angiotensin-aldosterone system.

281 erences in activity of the renin-angiotensin-aldosterone system.

282 l cortex and activates the renin-angiotensin-aldosterone system.

283 nd proteins related to the renin-angiotensin-aldosterone system; and (4) metabolism, associated with

284 nt CaV1.3 channels, the latter produced more aldosterone than wild-type, which was ameliorated by 100

285 P450 (P450) 11B2 catalyzes the formation of aldosterone, the major endogenous human mineralocorticoi

286 However, aldosterone, the physiological mineralocorticoid in huma

287 actol can explain why P450 11B2 must produce aldosterone through a processive mechanism despite favor

288 volve binding of the corticosteroid hormone, aldosterone to its mineralocorticoid receptor (MR).

289 ere screened for PA using the ratio of serum aldosterone to plasma renin activity.

290 Correspondingly, the aldosterone-to-renin ratio was positively and independen

291 cell mineralocorticoid receptor in CCDs from aldosterone-treated mice reduced chloride absorption and

292 18 hours in endotoxemic mice and restored in aldosterone-treated mice.

293 ted conditions, physiological stimulation of aldosterone was blunted with older age (beta=-4.6 ng/dL

294 oblasts, nuclear MR translocation induced by aldosterone was inhibited with NSC23766 and spironolacto

295 Urinary aldosterone was measured in participants in high sodium

296 In these stratified models, serum aldosterone was not a significant predictor of incident

297 rowth factor (CTGF) up-regulation induced by aldosterone was prevented with NSC23766.

298 Mean adjusted levels of urinary aldosterone were 6.5 mug/24 h (95% CI, 5.2 to 7.7 mug/24

299 ng values of plasma renin activity and serum aldosterone were 6.8 vs. 5.5 ng/mL/h (p = 0.002) and 654

300 ficiency increases angiotensin II (ATII) and aldosterone, which synergistically stimulate sodium rete