ライフサイエンスコーパス: aldosterone

1 were injected with lipopolysaccharide and/or aldosterone.

2 e-inactive TRPM7 mutant, was unresponsive to aldosterone.

3 pe, except for a 2.5-fold increase in plasma aldosterone.

4 ls to control the synthesis and secretion of aldosterone.

5 ZG but with an enhanced capacity to produce aldosterone.

6 o locus reached genome-wide significance for aldosterone.

7 nes, including the mineralocorticoid hormone aldosterone.

8 ssociated with strong stimulation of PRA and aldosterone.

9 ort of healthy persons receiving intravenous aldosterone (0.7 mug/kg per hour for 10 hours) versus ve

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

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

12 hat statin use may modulate the secretion of aldosterone, a well-known contributor to cardiovascular

13 Elevated levels of aldosterone activate Akt, and, in pulmonary arterial hyp

14 Aldosterone activates mineralocorticoid receptors (MRs)

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

16 tone, insulin resistance, renin-angiotensin-aldosterone activation, and inflammation lead to hyperki

17 Aldosterone affects serum potassium and is associated wi

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

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

20 4Cl treatment significantly decreased plasma aldosterone and antidiuretic hormone concentrations and

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

22 5R cells were transfected by ANO4 to measure aldosterone and CYP11B2 expression.

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

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

25 K1 into a NEDD4-2 substrate, thereby linking aldosterone and other NEDD4-2-suppressing antinatriureti

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

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

28 In contrast, aldosterone and the mineralocorticoid receptor (MR) prim

29 in vivo and in cultured cells that indicates aldosterone and vasopressin, the two major hormones regu

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

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

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

33 e of plasma potassium (p < 0.02), but plasma aldosterone, angiotensin II (ANGII), and renin activitie

34 erved Cardiac Function Heart Failure With an Aldosterone Antagonist (TOPCAT) and randomized to spiron

35 erved Cardiac Function Heart Failure With an Aldosterone Antagonist (TOPCAT) patients with heart fail

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

37 erved Cardiac Function Heart Failure With an Aldosterone Antagonist (TOPCAT) trial who were in sinus

38 nic heart failure in more than a decade: the aldosterone antagonist eplerenone in 2003 and a fixed do

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

40 tensin receptor blockers, beta-blockers, and aldosterone antagonists have improved mortality in patie

41 beta-blockers in 20.3% (50.5% of eligible), aldosterone antagonists in 24.1% (87.4% of eligible), hy

42 Aldosterone antagonists slow the progression of chronic

43 ngiotensin receptor blockers, beta-blockers, aldosterone antagonists, hydralazine/isosorbide dinitrat

44 ne excretion in these studies and found that aldosterone appeared to be the regulator for all 3 elect

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

46 inical validation for the lowering of plasma aldosterone as a viable approach to modulate blood press

47 ake drugs that inhibit the renin-angiotensin-aldosterone axis.

48 l relevance when interpreting the effects of aldosterone because the MR receptor is found in multiple

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

50 ed that lipophilic statins acutely inhibited aldosterone, but not corticosterone, in response to diff

51 tional zonation, essential for production of aldosterone by outer zona glomerulosa (ZG) and glucocort

52 as a potential to activate renin angiotensin aldosterone cascade to elevate blood pressure.

53 Conversely, low circulating aldosterone causes salt wasting and hypotension.

54 nearly 20-fold, which correlated with plasma aldosterone concentration and urinary Na/K ratio.

55 53311 with P<0.001 for both plasma renin and aldosterone concentration).

56 LS diet increased plasma renin activity and aldosterone concentration, whereas aldosterone infusion

57 whereas aldosterone infusion increased only aldosterone concentration.

58 P=0.001 for plasma renin, P=0.024 for plasma aldosterone concentration; and rs4253311 with P<0.001 fo

59 independent sample for both plasma renin and aldosterone concentrations (SNP rs5030062 in kininogen 1

60 Aldosterone concentrations and MR signalling are associa

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

62 Higher aldosterone concentrations were associated with lower se

63 With renin suppression, higher aldosterone concentrations were independently associated

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

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

66 d SGK1 on NCC, suggesting that WNK1 mediates aldosterone-dependent activity of the WNK/SPAK/OSR1 path

67 Aldosterone-dependent phosphorylation and degradation of

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

69 Known aldosterone driver mutations were identified in 8 of 23

70 d on human myotubes treated with MR agonist (aldosterone; EC50 1.3 nM) or antagonist (spironolactone;

71 d was inhibited by pharmacologic blockade of aldosterone effects with spironolactone (percentage of l

72 Functionally, 24-h aldosterone-enhanced SOCE is associated with increased d

73 king into consideration the so-called Ang II/aldosterone escape that often occurs after initial block

74 We monitored 24-h aldosterone excretion in these studies and found that al

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

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

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

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

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

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

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

82 Aldosterone improved 5-day survival, invasive arterial p

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

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

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

86 Long-term infusion of aldosterone in mice resulted in elevation of plasma inte

87 rotein expression, and direct measurement of aldosterone in tumor tissue, we confirmed the ability fo

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

89 Direct renin and aldosterone increased during pregnancy (both P < 0.001);

90 Further, aldosterone increased RENCA cell migration to a maximum

91 for the study of renal cell adenocarcinoma, aldosterone increased RENCA cell proliferation to a maxi

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

93 However, aldosterone-induced cardiac hypertrophy is totally preve

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

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

96 SGK1 blockade also prevented the aldosterone-induced increase of TRPM7 plasma membrane pr

97 proteasome system, an effect reversed by the aldosterone-induced kinase SGK1.

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

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

100 Inflammation is a key feature of aldosterone-induced vascular damage and dysfunction, but

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

102 ents NLRP3 and caspase-1 were protected from aldosterone-induced vascular damage.

103 t NLRP3 inflammasome plays a central role in aldosterone-induced vascular dysfunction.

104 get of rapamycin complex 1 subunit Raptor by aldosterone induces abnormal pulmonary artery smooth mus

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

106 ivity and aldosterone concentration, whereas aldosterone infusion increased only aldosterone concentr

107 he extent of pulmonary tumor spread, whereas aldosterone infusion recovered pulmonary metastatic spre

108 Dietary sodium restriction or acute aldosterone infusion similarly increased urine exosomal

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

110 n a murine model of HFpEF induced by chronic aldosterone infusion.

111 ertain medications such as renin angiotensin aldosterone inhibitors.

112 Notably, aldosterone interactions with both GR and MR demonstrate

113 ls of PAH in vivo Up-regulation of mTORC1 by aldosterone is a critical pathobiologic mechanism that c

114 Although aldosterone is a known regulator of renal and cardiovasc

115 Aldosterone is a major mineralocorticoid hormone that pl

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

117 Excess aldosterone is an important contributor to hypertension

118 ticoid-regulated kinase 1 mRNA expression by aldosterone is involved in enhanced SOCE.

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

120 ucocorticoids to increase MR selectivity for aldosterone, is also increased in dystrophic muscle tiss

121 d to potassium secretory segments, primed by aldosterone, kaliuresis results.

122 ineralocorticoid receptor (MR) activation by aldosterone leads to pathological myocardial signalling

123 SA and PA patients showed markedly elevated aldosterone levels (67 versus 39 ng/dL, respectively; no

124 Again, statin users had 26% lower aldosterone levels (P=0.006), particularly those using l

125 The very high plasma aldosterone levels detected under hypovolemic or hyperka

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

127 hic muscles compared with controls and local aldosterone levels in dystrophic skeletal muscles are in

128 Aldosterone levels positively correlated with the number

129 otassium diet (rescue diet), although plasma aldosterone levels remained significantly increased, NCC

130 nts of adrenal CYP11B2 expression and plasma aldosterone levels showed that increases in endogenous (

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

132 reased, and plasma renin activity and plasma aldosterone levels were decreased after the HS diet.

133 Cortisol and aldosterone levels were measured in samples from the adr

134 In secondary analyses, the lowest aldosterone levels were seen with lipophilic statins and

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

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

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

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

139 peutic interventions in conditions with high aldosterone levels.

140 rylation of NCC protein, despite high plasma aldosterone levels.

141 logical cardiac effects associated with high-aldosterone levels.

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

143 However, aldosterone may also stimulate the thiazide-sensitive Na

144 myeloid cells having the capacity to produce aldosterone may have implications for a wide variety of

145 ng, which suggests that mTORC1 regulation by aldosterone may mediate adverse pulmonary vascular remod

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

147 ess whether these effects were related to an aldosterone-mediated increase of TRPM7 current and/or pl

148 The aldosterone-mediated increase of TRPM7 current was inhib

149 Aldosterone mediates metastatic spread of renal cancer v

150 l (TRPC) and Orai1 channels are regulated by aldosterone/MR in neonatal rat ventricular cardiomyocyte

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

152 nin concentrations (n=8014), and circulating aldosterone (n=13289) from </=4 population-based cohorts

153 , renal wrap-induced hypertension, exogenous aldosterone; n=9) and young control dogs (sham surgery;

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

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

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

157 A or treated with spironolactone/eplerenone, aldosterone or pulmonary arterial plasma from patients w

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

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

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

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

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

163 Plasma renin activity, plasma aldosterone, plasma and 24 h urine sodium and potassium,

164 Since aldosterone plays a key role in vascular injury, the aim

165 We prospectively analyzed 20 patients with aldosterone producing adenoma (APA) that underwent adren

166 specificity test identified patients who has aldosterone producing adenoma (HR = 0.50, p = 0.005) als

167 Aldosterone producing adenomas (APAs) constitute a large

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

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

170 ion in treating primary aldosteronism due to aldosterone-producing adenoma (APA).

171 Aldosterone-producing adenomas (APAs) are benign tumors

172 Aldosterone-producing adenomas (APAs) vary in phenotype

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

174 Their aldosterone-producing adenomas harbored activating mutat

175 tion mutations in L-type CaV 1.3 channels in aldosterone-producing adenomas of patients with primary

176 Cell origin of aldosterone-producing adenomas, a major cause of hyperte

177 han 100 times as high as the levels in other aldosterone-producing adenomas.

178 In human aldosterone-producing adrenocortical cancer cell lines,

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

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

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

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

183 ransfected H295R cells, compound 8 decreased aldosterone production similar to high concentration of

184 s to increase CYP11B2 expression and enhance aldosterone production via calcium-dependent mechanisms.

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

186 ncoding aldosterone synthase) expression and aldosterone production.

187 contribute to the Ca(2+) signal that drives aldosterone production.

188 n tumor tissue, we confirmed the ability for aldosterone production.

189 rovide the primary Ca(2+) signal that drives aldosterone production.

190 creased intracellular Ca(2+), the signal for aldosterone production.

191 When overexpressed in vitro, it increases aldosterone production.

192 successful cannulation and lateralization of aldosterone production.

193 lated to tumorigenesis rather than excessive aldosterone production.

194 Our study provides the first evidence that aldosterone promotes TRPC1-, -C4-, -C5-, and Orai1-media

195 The renin-angiotensin-aldosterone (RAAS) and renal dopaminergic systems intera

196 6K, which provided a basis for investigating aldosterone-Raptor signaling in human PASMCs.

197 We hypothesized that aldosterone-Raptor signaling induces abnormal pulmonary

198 This study tested the hypothesis that aldosterone regulates cancer cell growth/spread via G pr

199 Aldosterone regulates electrolyte and fluid homeostasis

200 Aldosterone regulates sodium homeostasis by activating t

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

202 with genome-wide association results for the aldosterone/renin ratio in individuals of European ances

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

204 Furthermore, leptin-mediated aldosterone secretion contributes to cardiovascular dise

205 ANO4 overexpression in H295R cells increased aldosterone secretion from mean 0.9 pmol/mug protein (SE

206 Excess aldosterone secretion in patients with primary aldostero

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

208 receptors inhibition blunted leptin-induced aldosterone secretion.

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

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

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

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

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

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

215 alated cells, which are expressed within the aldosterone-sensitive region of the nephron, i.e., the d

216 , these findings provide strong evidence for aldosterone serving a causal role in renal cell cancer r

217 Aldosterone significantly increased after 6- and 12-mont

218 WT-TRPM7, we found that 18-h application of aldosterone significantly increased TRPM7 current and TR

219 In vitro, aldosterone stimulated NLRP3-dependent interleukin-1beta

220 Aldosterone-stimulated MR nuclear translocation was bloc

221 we hypothesized that APCCs have APA-related aldosterone-stimulating somatic gene mutations.

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

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

224 al studies conducted with LCI699 established aldosterone synthase (CYP11B2) inhibition as a promising

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

226 in rat telemetry studies and no increase of aldosterone synthase (CYP11B2) was detected in H295R cel

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

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

229 g classes, eg, inhibitors of vasopeptidases, aldosterone synthase and soluble epoxide hydrolase, agon

230 hat the C-allele containing genotypes of the aldosterone synthase CYP11B2 T(-344)C gene polymorphism

231 Aldosterone synthase protein levels are increased in leu

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

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

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

235 ll genes encoding enzymes in the pathway for aldosterone synthesis are expressed in muscle-derived le

236 Leptin is a newly described regulator of aldosterone synthesis that acts directly on adrenal glom

237 ctone = 26 +/- 8, P < 0.05) or inhibition of aldosterone synthesis with a high dietary salt diet (per

238 Aldosterone, synthesized in the adrenal cortex by the en

239 zyme inhibitors (ACEi) for renin-angiotensin-aldosterone system (RAAS) blockade are routinely used to

240 yte number is higher after renin-angiotensin-aldosterone system (RAAS) inhibition in glomerular disea

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

242 ncreased activation of the renin-angiotensin-aldosterone system (RAAS).

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

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

245 failure: activation of the renin-angiotensin-aldosterone system and decreased sensitivity to natriure

246 The renin-angiotensin-aldosterone system and members of the transforming growt

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

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

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

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

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

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

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

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

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

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

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

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

259 24 hours compared with non-renin-angiotensin-aldosterone system inhibitor patients.

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

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

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

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

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

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

266 ll as the potential use of renin-angiotensin-aldosterone system inhibitors in patients who were previ

267 ials testing the effect of renin-angiotensin-aldosterone system intervention on albuminuria class tra

268 Activation of the renin-angiotensin-aldosterone system is likely due, in part, to renal comp

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 ter-regulatory axis of the renin-angiotensin-aldosterone system previously demonstrated to have thera

272 been based on blocking the renin-angiotensin-aldosterone system with the use of angiotensin-convertin

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 eys, (2) activation of the renin-angiotensin-aldosterone system, and (3) increased sympathetic nervou

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

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

278 to activate the endogenous renin-angiotensin-aldosterone system.

279 edications that affect the renin-angiotensin-aldosterone system.

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

281 rials tested the effect of renin-angiotensin-aldosterone-system inhibitors and seven trials tested ot

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

283 suggests that the mineralocorticoid hormone aldosterone, through activation of its receptor, MR, mig

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

285 After RF ablation, CT images, aldosterone-to-renin ratio (ARR), serum potassium level,

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

287 ed a total of 47 plasma miRNAs and decreased aldosterone-to-renin ratios in the responder group (p =

288 18 hours in endotoxemic mice and restored in aldosterone-treated mice.

289 T-PCR and Western blotting demonstrated that aldosterone treatment for 24 h specifically increased th

290 Therefore, chronic aldosterone treatment increases the plasma membrane expr

291 sfunction, but molecular mechanisms by which aldosterone triggers inflammation remain unclear.

292 e, could be accounted for the high renin and aldosterone values, and the work overload associated wit

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

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

297 Recently, aldosterone was shown to increase intracellular Mg(2+) l

298 apacity to produce the natural ligand of MR, aldosterone, which in excess is known to exacerbate tiss

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

300 se-dependently raised CYP11B2 expression and aldosterone without elevating plasma angiotensin II, pot