ライフサイエンスコーパス: mineralocorticoid

1 n of aldosterone, the major endogenous human mineralocorticoid.

2 after physiologic or pharmacologic doses of mineralocorticoids.

3 -norprogesterone are potential physiological mineralocorticoids.

4 oxidative stress and sensitizes the heart to mineralocorticoid, accelerating hypertrophy, fibrosis, a

5 Whether mineralocorticoids act through H(+),K(+)-ATPases to main

6 and treatment of children with disorders of mineralocorticoid action are discussed.

7 licate interplay between direct and indirect mineralocorticoid actions in the distal nephron.

8 Consistent with this hypothesis, clamping mineralocorticoid activity at high levels unmasks greate

9 This study shows that, in humans, mineralocorticoid administration is associated with a ra

10 fusion of the synthetic mixed glucocorticoid/mineralocorticoid agonist prednisolone produced rapid in

11 RVENTIONS: Desoxycorticosterone, a selective mineralocorticoid agonist; dexamethasone, a selective gl

12 JECTS, AND Desoxycorticosterone, a selective mineralocorticoid agonist; dexamethasone, a selective gl

13 When inappropriate for salt status, the mineralocorticoid aldosterone induces cardiac and renal

14 The mineralocorticoid aldosterone is a major regulator of so

15 The mineralocorticoid aldosterone is produced in the adrenal

16 ) regulates blood volume by synthesizing the mineralocorticoid aldosterone.

17 The mineralocorticoid and androgen receptor antagonist spiro

18 gesterone receptors and has no effect on the mineralocorticoid and estrogen receptors in both yeast a

19 When compensated for mineralocorticoid and glucocorticoid deficiency, SR-BI/I

20 Corticosteroid regimens that stimulate both mineralocorticoid and glucocorticoid pathways consistent

21 synthesis and locally by actions on both the mineralocorticoid and glucocorticoid receptors, both of

22 ate osmolyte and water balance by rhythmical mineralocorticoid and glucocorticoid release, endogenous

23 his study was to determine whether exogenous mineralocorticoid and glucocorticoid treatments have dis

24 studied the effect of salt-driven changes in mineralocorticoid and glucocorticoid urinary excretion o

25 regulatory dominance for Na(+) transport of mineralocorticoids and defines the 'aldosterone-sensitiv

26 We aimed to study the effects of mineralocorticoids and the involvement of vascular miner

27 nery that is regulated by classical, nuclear mineralocorticoid, and glucocorticoid receptors.

28 have various alterations in glucocorticoid, mineralocorticoid, and sex steroid production that requi

29 but evidence supports the use of diuretics, mineralocorticoid antagonists and lifestyle intervention

30 electrophysiological and clinical effects of mineralocorticoid antagonists in myopathic hearts.

31 In septic shock, mineralocorticoids are only beneficial if given prophyla

32 despite inappropriately increased levels of mineralocorticoids, are incompletely understood.

33 neralocorticoid receptors are protected from mineralocorticoid binding by the absence of 11-beta hydr

34 rtical collecting duct, indirectly assessing mineralocorticoid bioactivity in patients who have hypo-

35 We previously showed that mineralocorticoid blockade improved CFR in men and women

36 Mineralocorticoid-coupled increases in free water reabso

37 istinguishing hyperkalemic patients who have mineralocorticoid deficiency versus resistance by observ

38 Administration of the mineralocorticoid deoxycorticosterone-acetate (DOCA) in

39 When inappropriate for salt status, mineralocorticoid (deoxycorticosterone acetate) excess c

40 Here, treatment of mice with the mineralocorticoid desoxycorticosterone pivalate (DOCP) r

41 In the renal collecting duct, mineralocorticoids drive Na(+) reabsorption, K(+) secret

42 We now report that glucocorticoids and mineralocorticoids effectively expand the CK5-positive c

43 othesis that high functional activity of the mineralocorticoid endocrine pathway contributes to vulne

44 rare autosomal recessive disorder, apparent mineralocorticoid excess (AME).

45 owever, the central contribution to Apparent Mineralocorticoid Excess and other hypertensive states i

46 The hypertensive syndrome of Apparent Mineralocorticoid Excess is caused by loss-of-function m

47 tubular acidosis, Liddle's disease, apparent mineralocorticoid excess syndrome and Bartter's type 3 s

48 at are used to treat side effects related to mineralocorticoid excess, can also bind to and activate

49 2) and thus exhibit the syndrome of apparent mineralocorticoid excess, provided an ideal model in whi

50 overload hypertrophy sensitizes the heart to mineralocorticoid excess, which promotes the transition

51 and blood pressure were examined in sham and mineralocorticoid excess-treated mice with a control die

52 acetate-producing bacteria independently of mineralocorticoid excess.

53 Compared with mineralocorticoid-excess mice fed a control diet, both h

54 balance was influenced by glucocorticoid and mineralocorticoid fluctuations.

55 We studied the effects of the mineralocorticoid fludrocortisone on the abundance of NC

56 aves glucocorticoid functions unaffected but mineralocorticoid functions increased, causing hypertens

57 of newly hatched fry, but not by estrogens, mineralocorticoids, glucocorticoids or progestogens.

58 Clamping mineralocorticoids high in Cx30(-/-) mice fed a high sod

59 ulation of salt transport in the kidney, the mineralocorticoid hormone aldosterone plays an independe

60 Accumulated evidence suggests that the mineralocorticoid hormone aldosterone, through activatio

61 egulated by numerous hormones, including the mineralocorticoid hormone aldosterone.

62 Recently, this mineralocorticoid hormone has been demonstrated to act o

63 Aldosterone is a major mineralocorticoid hormone that plays a key role in the r

64 However, aldosterone, the physiological mineralocorticoid in humans and other terrestrial verteb

65 des the well-known roles of aldosterone as a mineralocorticoid in regulating homeostasis of electroly

66 ol functioned as both a glucocorticoid and a mineralocorticoid in the lamprey.

67 Exogenous mineralocorticoid increases ENaC activity equally well i

68 focused on salt/nephrectomy in accelerating mineralocorticoid-induced cardiac effects, we hypothesiz

69 r injury, and kidney fibrosis with aging and mineralocorticoid-induced hypertension.

70 f 11-beta hydroxysteroid dehydrogenase, salt-mineralocorticoid-induced inflammation is postulated to

71 n steroidogenesis, controlling the levels of mineralocorticoids influencing blood pressure, glucocort

72 tatory stimulus of salt appetite mediated by mineralocorticoids is abolished by PBN lesions.

73 gic projections and expresses high levels of mineralocorticoid (MR) and glucocorticoid (GR) receptors

74 idepressant-induced increases in hippocampal mineralocorticoid (MR) and glucocorticoid receptor (GR)

75 Removal of endogenous glucocorticoids and mineralocorticoids neither augmented nor lessened the hy

76 ses-play an important role in the effects of mineralocorticoids on K(+), acid-base, and Na(+) balance

77 We found a beneficial effect of mineralocorticoids on survival, blood pressure, and vasc

78 Adrenal expression of the genes for mineralocorticoid-producing enzymes ranged from 50% norm

79 one stimulates fibronectin synthesis through mineralocorticoid receptor (MCR) dependent activation of

80 Here we show that mineralocorticoid receptor (MR) activation by aldosteron

81 erations in glucocorticoid receptor (GR) and mineralocorticoid receptor (MR) activation drive compuls

82 dent aldosteronism that results in excessive mineralocorticoid receptor (MR) activation.

83 with hormone replacement with the selective mineralocorticoid receptor (MR) agonist aldosterone, the

84 the steroid hormone aldosterone, which is a mineralocorticoid receptor (MR) agonist, is associated w

85 Because adipocytes express mineralocorticoid receptor (MR) and MR blockade reduces

86 In rodents, mineralocorticoid receptor (MR) antagonism prevents AKI

87 ly, renin-angiotensin-aldosterone system and mineralocorticoid receptor (MR) antagonism reduces cardi

88 the administration of the novel nonsteroidal mineralocorticoid receptor (MR) antagonist BR-4628 can p

89 , was recently reported to possess excellent mineralocorticoid receptor (MR) antagonist in vitro pote

90 n converting enzyme inhibitor lisinopril and mineralocorticoid receptor (MR) antagonist spironolacton

91 ion, or that were treated with the selective mineralocorticoid receptor (MR) antagonist spironolacton

92 Here we report that treatment with the oral mineralocorticoid receptor (MR) antagonist spironolacton

93 mortality has led to increased interest in a mineralocorticoid receptor (MR) antagonist-based treatme

94 Mineralocorticoid receptor (MR) antagonists are effectiv

95 Mineralocorticoid receptor (MR) antagonists are the reco

96 Steroidal mineralocorticoid receptor (MR) antagonists are used for

97 FDA-approved mineralocorticoid receptor (MR) antagonists are used to

98 A novel series of nonsteroidal mineralocorticoid receptor (MR) antagonists identified a

99 cal and experimental studies have shown that mineralocorticoid receptor (MR) antagonists substantiall

100 ears as an alternative therapeutic option to mineralocorticoid receptor (MR) antagonists to reduce el

101 These effects were dependent on the mineralocorticoid receptor (MR) as they were abolished b

102 e aim of this study was to determine whether mineralocorticoid receptor (MR) blockade improves CFR in

103 TRPM7 current was inhibited by eplerenone, a mineralocorticoid receptor (MR) blocker, and GSK-650394,

104 Spironolactone, a nonselective mineralocorticoid receptor (MR) blocker, antagonizes ald

105 tective effects of Ly, a novel non-steroidal mineralocorticoid receptor (MR) blocker, through two exp

106 Mineralocorticoid receptor (MR) drugs have been used cli

107 ects on GR or TH expression in the VTA or on mineralocorticoid receptor (MR) expression in any of the

108 Mineralocorticoid receptor (MR) expression is increased

109 s shift may be mediated by activation of the mineralocorticoid receptor (MR) for cortisol.

110 1 mice also unexpectedly exhibited increased mineralocorticoid receptor (MR) gene expression.

111 We studied the role of the mineralocorticoid receptor (MR) in the signaling that pr

112 Here, we targeted the role of the mineralocorticoid receptor (MR) in the stress-induced mo

113 The mineralocorticoid receptor (MR) is a nuclear receptor an

114 The mineralocorticoid receptor (MR) is highly conserved acro

115 Activation of the mineralocorticoid receptor (MR) may promote dysfunctiona

116 The mineralocorticoid receptor (MR) mediates the Na(+)-retai

117 Phosphorylation of human mineralocorticoid receptor (MR) on Ser-843, a residue pl

118 In contrast, aldosterone and the mineralocorticoid receptor (MR) primarily promote cardio

119 rials have emphasized the beneficial role of mineralocorticoid receptor (MR) signaling blockade in he

120 s thought to be caused by an exacerbation of mineralocorticoid receptor (MR) signaling, given that it

121 f nonsteroidal pyrazoline antagonists of the mineralocorticoid receptor (MR) that show excellent pote

122 d hormone aldosterone acts by binding to the mineralocorticoid receptor (MR), a ligand-activated tran

123 gulates sodium homeostasis by activating the mineralocorticoid receptor (MR), a member of the nuclear

124 The mineralocorticoid receptor (MR), acting in the kidney, i

125 r beta (Esr2), glucocorticoid receptor (Gr), mineralocorticoid receptor (Mr), and progesterone recept

126 receptor (ER), glucocorticoid receptor (GR), mineralocorticoid receptor (MR), and progesterone recept

127 eptors, the glucocorticoid receptor (GR) and mineralocorticoid receptor (MR), both of which are prese

128 aggravate CSCR and are known to bind to the mineralocorticoid receptor (MR), CSCR may be related to

129 affect the overall transcription of CRH, the mineralocorticoid receptor (MR), the serotonin transport

130 nsequence of mutations in genes encoding the mineralocorticoid receptor (MR), the three subunits of t

131 characterize the role of Rac1 GTPase for the mineralocorticoid receptor (MR)-mediated pro-fibrotic re

132 e corticosteroid hormone, aldosterone to its mineralocorticoid receptor (MR).

133 Although spironolactone can act at the mineralocorticoid receptor (MR; NR3C2), there is increas

134 s in the glucocorticoid receptor (NR3C1) and mineralocorticoid receptor (NR3C2) genes with cCSC.

135 Intercalated cell mineralocorticoid receptor ablation blunted, but did not

136 h circulating aldosterone, intercalated cell mineralocorticoid receptor ablation reduces chloride abs

137 d/or oxidative stress may also contribute to mineralocorticoid receptor activation in obesity.

138 However, obesity also causes mineralocorticoid receptor activation independent of ald

139 through transcriptional mechanisms involving mineralocorticoid receptor activation.

140 , tumor necrosis factor-alpha decreased both mineralocorticoid receptor and alpha1-adrenoceptor expre

141 harmacological studies and demonstrated both mineralocorticoid receptor and glucocorticoid receptor p

142 pendent nuclear translocation and binding of mineralocorticoid receptor and glucocorticoid receptor t

143 Therefore, central mineralocorticoid receptor antagonism could increase com

144 In human pulmonary artery endothelial cells, mineralocorticoid receptor antagonism with spironolacton

145 receptor antagonist pretreatment and not by mineralocorticoid receptor antagonism, suggesting a gluc

146 esting with evidence-based treatment using a mineralocorticoid receptor antagonist (MRA) and with lon

147 prilysin inhibitor (ARNI), beta-blocker, and mineralocorticoid receptor antagonist (MRA) were examine

148 nd renal function in patients treated with a mineralocorticoid receptor antagonist (MRA).

149 tics (yes/no), digitalis glycoside (yes/no), mineralocorticoid receptor antagonist (yes/no),and defib

150 Here we demonstrate that spironolactone, a mineralocorticoid receptor antagonist approved for clini

151 e intestinal peptide receptor 2, and a novel mineralocorticoid receptor antagonist are in phase II/II

152 angiotensin receptor-neprilysin inhibitor+BB+mineralocorticoid receptor antagonist combination therap

153 (-)-Finerenone is a nonsteroidal mineralocorticoid receptor antagonist currently in phase

154 iomethylspironolactone nor the more specific mineralocorticoid receptor antagonist eplerenone affecte

155 We evaluated the effect of the selective mineralocorticoid receptor antagonist eplerenone on rena

156 induced changes were blocked by applying the mineralocorticoid receptor antagonist eplerenone.

157 ed the effect of the nonsteroidal, selective mineralocorticoid receptor antagonist finerenone on kidn

158 as foundational therapy, with addition of a mineralocorticoid receptor antagonist in patients with p

159 articipants, was prespecified as part of the Mineralocorticoid Receptor Antagonist in Type 2 Diabetes

160 We show here that the mineralocorticoid receptor antagonist spironolactone red

161 adding an angiotensin receptor blocker or a mineralocorticoid receptor antagonist to a regimen based

162 angiotensin receptor-neprilysin inhibitor+BB+mineralocorticoid receptor antagonist to implantable car

163 n angiotensin-converting enzyme inhibitor or mineralocorticoid receptor antagonist was associated wit

164 angiotensin-converting enzyme inhibitor or a mineralocorticoid receptor antagonist will decrease the

165 iotensin receptor blocker, beta-blocker, and mineralocorticoid receptor antagonist) and outcomes of p

166 ementing HK-fed Kcnmb1(-/-) with eplerenone (mineralocorticoid receptor antagonist) corrected the flu

167 In addition, 4671 (56%) were treated with a mineralocorticoid receptor antagonist, 2539 (30%) with d

168 Previous research suggests the mineralocorticoid receptor antagonist, eplerenone, is ef

169 ardiac defibrillator+ACE inhibitor or ARB+BB+mineralocorticoid receptor antagonist, implantable cardi

170 Finerenone, a nonsteroidal, selective mineralocorticoid receptor antagonist, reduced albuminur

171 iotensin receptor blocker, beta-blocker, and mineralocorticoid receptor antagonist, respectively.

172 We assessed the risk factors for mineralocorticoid receptor antagonist-related WRF and fo

173 ker, renin-angiotensin system inhibitor, and mineralocorticoid receptor antagonist; 40.3% versus 30.4

174 ngiotensin II receptor blockers (84.2%), and mineralocorticoid receptor antagonists (57.0%).

175 <95 mm Hg received significantly more often mineralocorticoid receptor antagonists (64.5% versus 43.

176 Mineralocorticoid receptor antagonists (MRA) improve out

177 Mineralocorticoid receptor antagonists (MRA) reduce morb

178 receptor blockers (ARB), beta-blockers (BB), mineralocorticoid receptor antagonists (MRA), and angiot

179 Consensus guidelines recommend the use of mineralocorticoid receptor antagonists (MRAs) for select

180 Mineralocorticoid receptor antagonists (MRAs) have becom

181 Mineralocorticoid receptor antagonists (MRAs) may attenu

182 The mineralocorticoid receptor antagonists (MRAs) spironolac

183 Three drug classes (mineralocorticoid receptor antagonists [MRAs], angiotens

184 Mineralocorticoid receptor antagonists administered at h

185 Mineralocorticoid receptor antagonists are a valuable ad

186 These findings suggest that the use of mineralocorticoid receptor antagonists coupled with GC t

187 beta-Blockers, calcium channel blockers, and mineralocorticoid receptor antagonists did not achieve s

188 Mineralocorticoid receptor antagonists improve outcomes

189 ace, but whether race influences efficacy of mineralocorticoid receptor antagonists in heart failure

190 in II receptor blockers, ACE inhibitors, and mineralocorticoid receptor antagonists increase ACE2 rec

191 findings suggest that safety and efficacy of mineralocorticoid receptor antagonists may differ by rac

192 The incidence of hyperkalemia caused by mineralocorticoid receptor antagonists may vary by race,

193 rimary objective was to assess the impact of mineralocorticoid receptor antagonists on cardiovascular

194 Mineralocorticoid receptor antagonists reduce morbidity

195 zed controlled trials in heart failure (HF), mineralocorticoid receptor antagonists reduced mortality

196 Mineralocorticoid receptor antagonists were independentl

197 Mineralocorticoid receptor antagonists were prescribed i

198 ism (e.g., thiazide-type diuretic agents and mineralocorticoid receptor antagonists) should be avoide

199 receptor blockers (ARBs), beta blockers, and mineralocorticoid receptor antagonists, and advanced dev

200 ors, Ang II type 1 receptor antagonists, and mineralocorticoid receptor antagonists, are a cornerston

201 , N-terminal pro-B-type natriuretic peptide, mineralocorticoid receptor antagonists, low voltage, ine

202 antagonist G-36, but was not affected by the mineralocorticoid receptor antagonists, spironolactone a

203 g body of evidence has suggested benefits of mineralocorticoid receptor antagonists, such as eplereno

204 Mineralocorticoid receptor antagonists, such as spironol

205 with heart failure and may be attenuated by mineralocorticoid receptor antagonists.

206 eta-blockers, and 32% (95% CI: 25%-39%) with mineralocorticoid receptor antagonists.

207 ocked by the GPER antagonist, but not by the mineralocorticoid receptor antagonists.

208 rolytes in patients with AF and HF receiving mineralocorticoid receptor antagonists.

209 s of beta-blocker, sacubitril/valsartan, and mineralocorticoid receptor antagonists.

210 edical therapies including beta-blockers and mineralocorticoid receptor antagonists.

211 In contrast, an antagonist of the mineralocorticoid receptor as well as agonists of proges

212 Although we have known that mineralocorticoid receptor blockade attenuates cardiovas

213 Mineralocorticoid receptor blockade before stress preven

214 Mineralocorticoid receptor blockade blunted leptin-induc

215 angiotensin-converting enzyme inhibition nor mineralocorticoid receptor blockade decreased the primar

216 l injury, only recently have we learned that mineralocorticoid receptor blockade improves pancreatic

217 T(1) receptor blockade using candesartan and mineralocorticoid receptor blockade using canrenoic acid

218 oxygen consumption, which was normalized by mineralocorticoid receptor blockade.

219 Mineralocorticoid receptor blockers have been shown to b

220 genetic causes of primary aldosteronism, and mineralocorticoid receptor blockers have now become an i

221 needs to be achieved in exploring the use of mineralocorticoid receptor blockers in less advanced sta

222 attributed to promiscuous activation of the mineralocorticoid receptor by cortisol, thereby promotin

223 2), allowing inappropriate activation of the mineralocorticoid receptor by endogenous glucocorticoid.

224 ium channel activity, despite principal cell mineralocorticoid receptor expression in the knockout mi

225 Furthermore, blunted vascular mineralocorticoid receptor expression might participate

226 Mineralocorticoid receptor expression was also blunted i

227 Both alpha1-adrenoceptor and mineralocorticoid receptor expressions studied in mouse

228 d by a persistent enhancement in hippocampal mineralocorticoid receptor function.

229 h circulating aldosterone, intercalated cell mineralocorticoid receptor gene ablation directly reduce

230 -jun, which forms a nuclear complex with the mineralocorticoid receptor in a kidney fibroblast cell l

231 Ablation of the intercalated cell mineralocorticoid receptor in CCDs from aldosterone-trea

232 enetic study support a possible role for the mineralocorticoid receptor in the pathogenesis of cCSC.

233 D in the presence of NKCC1, K(+) channel and mineralocorticoid receptor inhibitors, revealed interact

234 This study assessed whether the mineralocorticoid receptor iso/val polymorphism (rs5522)

235 in wild-type and intercalated cell-specific mineralocorticoid receptor knockout mice.

236 Vitamin D receptor, oestrogen receptor and mineralocorticoid receptor modulators regulate podocyte

237 its antitumor effects are independent of the mineralocorticoid receptor pathway.

238 ndent of blood pressure, but the role of the mineralocorticoid receptor remains unclear.

239 sequences of aldosterone excess require full mineralocorticoid receptor signaling.

240 ENaC transcription independent of effects on mineralocorticoid receptor trans-activation.

241 ng to Nguyen et al., local inhibition of the mineralocorticoid receptor via antagonists (spironolacto

242 nfirmed by pharmacological inhibition of the mineralocorticoid receptor with spironolactone or eplere

243 ong-acting thiazide-like diuretic and an MR (mineralocorticoid receptor) antagonist, at maximal or ma

244 do) promotes fibrosis in myocardium, and MR (mineralocorticoid receptor) antagonists (MRAs) improve c

245 The glucocorticoid receptor and the mineralocorticoid receptor, 2 glucocorticoid-binding rec

246 ding alterations in Na(+)/K(+)-ATPase, WNK1, mineralocorticoid receptor, and NEDD4L expression, as we

247 gen receptor alpha, glucocorticoid receptor, mineralocorticoid receptor, and progesterone receptor) a

248 tin, estrogen, androgen, glucocorticoid, and mineralocorticoid receptor, as well as sex hormone and c

249 ype b receptor, angiotensin type 1 receptor, mineralocorticoid receptor, or Nox isoforms 1 to 4.

250 Aldosterone activates the intercalated cell mineralocorticoid receptor, which is enhanced with hypok

251 CC1 and outward K(+) channels, mediated by a mineralocorticoid receptor-ALD complex.

252 tructure and function, oxidative stress, and mineralocorticoid receptor-dependent gene transcription

253 d ejection fraction independently of classic mineralocorticoid receptor-dependent gene transcription.

254 across the groups but no evidence of classic mineralocorticoid receptor-dependent gene transcription.

255 ressure response to dietary sodium through a mineralocorticoid receptor-dependent pathway.

256 id receptor, they also bind and activate the mineralocorticoid receptor.

257 an be remedied by blocking activation of the mineralocorticoid receptor.

258 s sensitive to antagonism of GPER but not of mineralocorticoid receptor.

259 roate antagonism versus agonism in the human mineralocorticoid receptor.

260 nt PHAI is characterized by mutations in the mineralocorticoid receptor.

261 ediated in part by aldosterone acting on the mineralocorticoid receptor.

262 3C1 (glucocorticoid receptor; GR) and NR3C2 (mineralocorticoid receptor; MR) that encode for GRs and

263 rein all patients with RH are treated with a mineralocorticoid-receptor antagonist without further te

264 Mineralocorticoid-receptor antagonists improve the progn

265 tensin-receptor blockers, beta-blockers, and mineralocorticoid-receptor antagonists.

266 receptors (eg, atrasentan) and non-steroidal mineralocorticoid receptors (eg, finerenone).

267 on of glucocorticoid hormones, which bind to mineralocorticoid receptors (MRs) and glucocorticoid rec

268 Mineralocorticoid receptors (MRs) in the brain play a ro

269 termine which brain receptors [high-affinity mineralocorticoid receptors (MRs) or low-affinity glucoc

270 Aldosterone activates mineralocorticoid receptors (MRs) to increase epithelial

271 a steroid hormone that signals through renal mineralocorticoid receptors (MRs) to regulate blood pres

272 chanism by which glucocorticoids, acting via mineralocorticoid receptors (MRs), decrease resilience t

273 and fluid homeostasis through binding to the mineralocorticoid receptors (MRs).

274 CC1 protein expression via the activation of mineralocorticoid receptors and post-transcriptional mod

275 nne muscular dystrophy mouse models and that mineralocorticoid receptors are present and functional i

276 Because cardiac mineralocorticoid receptors are protected from mineraloc

277 Consistently, blockade of mineralocorticoid receptors by spironolactone treatment

278 ucocorticoid synthesis or glucocorticoid and mineralocorticoid receptors enabled the expression of em

279 locorticoids and the involvement of vascular mineralocorticoid receptors in murine endotoxic and huma

280 e recently discovered interaction of GC with mineralocorticoid receptors may counteract negative effe

281 e receptors-2 mGlu2, neuropeptide-Y NPY, and mineralocorticoid receptors MR).

282 Vascular mineralocorticoid receptors play a role in vascular tone

283 In addition to acting on mineralocorticoid receptors, aldosterone has been recent

284 result of cortisol depletion of the cerebral mineralocorticoid receptors.

285 Grade 3 or 4 mineralocorticoid-related adverse events and abnormaliti

286 Mineralocorticoid-related adverse events, including flui

287 The incidence of mineralocorticoid-related toxicities (hypertension or hy

288 alt intake decreased the level of rhythmical mineralocorticoid release and elevated rhythmical glucoc

289 lt intake, half-weekly and weekly rhythmical mineralocorticoid release promoted free water reabsorpti

290 SR-BI/II(-/-) mice with mineralocorticoid replacement demonstrated an approximat

291 specific pseudohypoaldosteronism type 1 with mineralocorticoid resistance without evidence of impaire

292 Prophylactic mineralocorticoids should be further investigated in pat

293 ons suggest that the conventional concept of mineralocorticoid signaling in the DCT should be revised

294 ENaC Po persist in the presence of saturated mineralocorticoid status.

295 action of aldosterone and potentially other mineralocorticoid steroids has been increasingly demonst

296 esting and empirical low-dose glucocorticoid/mineralocorticoid supplementation in children with syste

297 ated sodium transport in mCCD cells, without mineralocorticoid supplementation.

298 multiple levels, systemically by increasing mineralocorticoid synthesis and locally by actions on bo

299 superfamily, responding to glucocorticoids, mineralocorticoids, thyroid hormone, and vitamin D.

300 es in circulating androgens and increases in mineralocorticoids were seen with all doses.