ライフサイエンスコーパス: mineralocorticoid

1 after physiologic or pharmacologic doses of mineralocorticoids.

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

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

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

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

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

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

8 dium appetite are both stimulated by chronic mineralocorticoid administration.

9 dium deficiency, which does not occur during mineralocorticoid administration.

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 ) regulates blood volume by synthesizing the mineralocorticoid aldosterone.

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

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

18 Corticosteroid regimens that stimulate both mineralocorticoid and glucocorticoid pathways consistent

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

20 erone replacement, suggesting a synergism of mineralocorticoid and glucocorticoid receptors.

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

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

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

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

25 that is essential for adrenal production of mineralocorticoids and glucocorticoids.

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 Mineralocorticoid antagonists have emerged as a new para

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 Mineralocorticoid-coupled increases in free water reabso

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

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

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

39 In a model of mineralocorticoid-dependent hypertension involving chron

40 in the heart as well as the fibrosis seen in mineralocorticoid-dependent hypertension.

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

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

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

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

45 osis and illustrates the supportive roles of mineralocorticoids, endothelin, and novel signaling path

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

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

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

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

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

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

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

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

54 acetate-producing bacteria independently of mineralocorticoid excess.

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

56 balance was influenced by glucocorticoid and mineralocorticoid fluctuations.

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

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

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

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

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

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

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

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

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

66 ial dysfunction by reducing O2- in low renin mineralocorticoid hypertension.

67 an ET(A)/NADPH oxidase pathway in low-renin mineralocorticoid hypertension.

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

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

70 Exogenous mineralocorticoid increases ENaC activity equally well i

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

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

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

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

75 Aldosterone, the principal human mineralocorticoid, is increasingly recognized as playing

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

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

78 Additional studies evaluated the role of mineralocorticoid (MR) and glucocorticoid receptor (GR)

79 cursor of vertebrate glucocorticoid (GR) and mineralocorticoid (MR) receptors.

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

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

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

83 In conclusion, either mineralocorticoids or glucocorticoids can downregulate U

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

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

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

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

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

89 g is the first step in hormone regulation of mineralocorticoid receptor (MR) activity.

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

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

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

93 l function are thought to be mediated by the mineralocorticoid receptor (MR) and the glucocorticoid r

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

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

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

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

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

99 rofibrotic effects, respectively, as did the mineralocorticoid receptor (MR) antagonist spironolacton

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

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

102 Mineralocorticoid receptor (MR) antagonists are the reco

103 Steroidal mineralocorticoid receptor (MR) antagonists are used for

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

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

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

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

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

109 as a deleterious hormone in the heart, with mineralocorticoid receptor (MR) blockade reducing mortal

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

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

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

113 Mineralocorticoid receptor (MR) controls sodium homeosta

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

115 Mineralocorticoid receptor (MR) expression is increased

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

117 1 mice also unexpectedly exhibited increased mineralocorticoid receptor (MR) gene expression.

118 After a survey of the entire brain for mineralocorticoid receptor (MR) immunoreactivity, we dis

119 and anxiety disorders, the role of the brain mineralocorticoid receptor (MR) in stress, depression, a

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

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

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

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

124 trogen receptor alpha (ERalpha), but not the mineralocorticoid receptor (MR) or ERbeta.

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

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

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

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

129 Both stereoisomers bind to the mineralocorticoid receptor (MR) with a Ki value of appro

130 coid response [glucocorticoid receptor (GR), mineralocorticoid receptor (MR), 11beta-hydroxysteroid d

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

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

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

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

135 y cultures demonstrated specific GR, but not mineralocorticoid receptor (MR), activation and phosphor

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

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

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

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

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

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

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

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

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

145 through transcriptional mechanisms involving mineralocorticoid receptor activation.

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

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

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

149 treatment of patients with a combination of mineralocorticoid receptor antagonism (eplerenone) and a

150 mechanistic investigations have established mineralocorticoid receptor antagonism as the new treatme

151 Therefore, central mineralocorticoid receptor antagonism could increase com

152 le that, along with ACE-I and beta-blockers, mineralocorticoid receptor antagonism will become part o

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

154 Mineralocorticoid receptor antagonism, but not PAI-1 def

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

156 fine better the biologic mechanisms by which mineralocorticoid receptor antagonisms exert the observe

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

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

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

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

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

162 lopment of CV injury were assessed using the mineralocorticoid receptor antagonist spironolactone (0,

163 The mineralocorticoid receptor antagonist spironolactone inh

164 We show here that the mineralocorticoid receptor antagonist spironolactone red

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

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

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

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

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

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

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

172 Mineralocorticoid receptor antagonists (MRA) improve out

173 Mineralocorticoid receptor antagonists (MRA) reduce morb

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

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

176 Mineralocorticoid receptor antagonists (MRAs) have becom

177 Mineralocorticoid receptor antagonists (MRAs) may attenu

178 The mineralocorticoid receptor antagonists (MRAs) spironolac

179 Mineralocorticoid receptor antagonists administered at h

180 Mineralocorticoid receptor antagonists are a valuable ad

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

182 Mineralocorticoid receptor antagonists improve outcomes

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

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

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

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

187 Mineralocorticoid receptor antagonists reduce morbidity

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

189 Mineralocorticoid receptor antagonists were independentl

190 Mineralocorticoid receptor antagonists were prescribed i

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

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

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

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

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

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

197 Mineralocorticoid receptor antagonists, such as spironol

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

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

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

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

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

203 Although we have known that mineralocorticoid receptor blockade attenuates cardiovas

204 Mineralocorticoid receptor blockade before stress preven

205 Mineralocorticoid receptor blockade blunted leptin-induc

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

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

208 Mineralocorticoid receptor blockers have been shown to b

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

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

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

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

213 id receptor did not, and studies with rat GR-mineralocorticoid receptor chimeras confirmed that the G

214 repressed TGF-beta transactivation, whereas mineralocorticoid receptor did not, and studies with rat

215 Furthermore, blunted vascular mineralocorticoid receptor expression might participate

216 Mineralocorticoid receptor expression was also blunted i

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

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

219 Mutations in the mineralocorticoid receptor gene (MR) cause adPHA1, but t

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

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

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

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

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

225 sequences of aldosterone excess require full mineralocorticoid receptor signaling.

226 The effects of mineralocorticoid receptor stimulation are associated wi

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

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

229 Finally, antagonism of the mineralocorticoid receptor will attenuate or abrogate ma

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

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

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

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

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

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

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

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

238 uses cardiovascular and renal injury through mineralocorticoid receptor-dependent mechanisms.

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

240 roid hormone aldosterone and its partner the mineralocorticoid receptor-evolved by a stepwise Darwini

241 We used the mineralocorticoid receptor-selective antagonist eplereno

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

243 roate antagonism versus agonism in the human mineralocorticoid receptor.

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

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

246 progesterone-mediated activation of a mutant mineralocorticoid receptor.

247 icating that aldosterone was working via the mineralocorticoid receptor.

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

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

250 3C1 (glucocorticoid receptor; GR) and NR3C2 (mineralocorticoid receptor; MR) that encode for GRs and

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

252 Mineralocorticoid-receptor antagonists improve the progn

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

254 xis occurs through a dual-receptor system of mineralocorticoid receptors (MR) and glucocorticoid rece

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

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

257 Blocking brain mineralocorticoid receptors (MRs) reduces the high circu

258 Aldosterone activates mineralocorticoid receptors (MRs) to increase epithelial

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

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

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

262 These neurons express mineralocorticoid receptors and the enzyme 11-beta-hydro

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

264 Because cardiac mineralocorticoid receptors are protected from mineraloc

265 Consistently, blockade of mineralocorticoid receptors by spironolactone treatment

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

267 le is known about the role of aldosterone or mineralocorticoid receptors in mediating adverse remodel

268 agonist eplerenone (EPL) to test the role of mineralocorticoid receptors in mediating the transition

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

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

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

272 Vascular mineralocorticoid receptors play a role in vascular tone

273 Mineralocorticoid receptors play an important role in me

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

275 Although aldosterone, acting via mineralocorticoid receptors, causes left ventricular (LV

276 uate aldosterone activation of cardiomyocyte mineralocorticoid receptors, transgenic mice overexpress

277 t cell line that stably expresses functional mineralocorticoid receptors.

278 result of cortisol depletion of the cerebral mineralocorticoid receptors.

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

280 Mineralocorticoid-related adverse events, including flui

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

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

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

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

285 d life-saving glucocorticoid-replacement and mineralocorticoid-replacement therapy, health-related qu

286 steroids, but not mouse glucocorticoids and mineralocorticoids, requires P450c17, which catalyzes bo

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

288 lay a significant role in the development of mineralocorticoid-salt hypertension.

289 These neurons are mineralocorticoid-sensitive and are activated in associa

290 Prophylactic mineralocorticoids should be further investigated in pat

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

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

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

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

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

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

297 l insufficiency." Replacement glucocorticoid/mineralocorticoid therapy over 7 days appears to be bene

298 and benefit from replacement glucocorticoid/mineralocorticoid therapy.

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.