ライフサイエンスコーパス: spironolactone

1 for any reason were significantly reduced by spironolactone.

2 aldosterone was inhibited with NSC23766 and spironolactone.

3 (n=6551) or were not (n=12 301) treated with spironolactone.

4 easing evidence of MR-independent effects of spironolactone.

5 mulation was blocked by mifepristone but not spironolactone.

6 d to evaluate amiloride as an alternative to spironolactone.

7 r a previous large fall in blood pressure on spironolactone.

8 angiotensin-converting enzyme inhibitors or spironolactone.

9 pokalemia (<3.4 mmol/l) that were rescued by spironolactone.

10 al of 840 patients had new prescriptions for spironolactone.

11 ravated with furosemide and is attenuated by spironolactone.

12 is blocked by the competitive MR antagonist spironolactone.

13 and (3) adrenalectomy plus dexamethasone and spironolactone.

14 e mineralocorticoid receptor (MR) antagonist spironolactone.

15 also treated with beta blockers and 17% with spironolactone.

16 y define a subgroup with warranting trial of spironolactone.

17 Salt appetite was inhibited by spironolactone.

18 ase 9 inhibition, and myocardial fibrosis by spironolactone.

19 heart failure were significantly reduced by spironolactone.

20 n of MR are inhibited by both finerenone and spironolactone.

21 annels could be a relevant in vivo target of spironolactone.

22 ear accumulation of MR more efficiently than spironolactone.

23 ine and reduced by the antihypertensive drug Spironolactone.

24 dine-derived selective MR antagonist, and by spironolactone.

25 ng the mineralocorticoid receptor antagonist spironolactone (0, 1.5, 15, and 50 mg x 100 g(-1) x day(

26 Patients in the ramipril (0.7%) or spironolactone (0.7%) group were less likely to develop

27 tic/ACE inhibitor therapy, comparing 50 mg/d spironolactone (1 month) versus placebo.

28 ntrast, 24 h exposure with the MR antagonist spironolactone (1-10 microM), the GR antagonist RU-486 (

29 Spironolactone 100 mg and bendroflumethiazide 5 mg cause

30 bendroflumethiazide 5 mg was as effective as spironolactone 100 mg in lowering blood pressure, despit

31 High-dose spironolactone (100 mg) vs placebo or 25 mg spironolacto

32 on fraction of 45% or more to receive either spironolactone (15 to 45 mg daily) or placebo.

33 ombination with an ALDO receptor antagonist, spironolactone (200 mg/kg p.o. daily), or an antioxidant

34 , and four weeks of ALDO/salt + furosemide + spironolactone (200 mg/kg/day in divided doses by twice-

35 re frequently in survivors with PLE included spironolactone (21 [68%]), octreotide (7 [21%]), sildena

36 body wt per d) (group 2), or furosemide plus spironolactone (22 and 20 mg/100 g body wt per d, respec

37 ailure guidelines were randomized to receive spironolactone 25 mg daily or placebo in a double-blind

38 After an active run-in phase with spironolactone 25 mg once daily, 112 patients with stage

39 n fraction <35% randomized to treatment with spironolactone 25 mg or placebo in the Randomized Aldact

40 mg/day) were randomized to add-on therapy of spironolactone 25 mg, hydrochlorothiazide (HCTZ) 12.5 mg

41 Participants were randomized to spironolactone 25 mg, which could be titrated to 50 mg,

42 zed stepped-care antihypertensive treatment, spironolactone 25 mg/d, bisoprolol 10 mg/d, prazosin 5 m

43 Patients were randomized to 6 months of oral spironolactone 25 mg/day or matching placebo.

44 ents to placebo, losartan (100 mg daily), or spironolactone (25 mg daily) for 48 wk.

45 tassium canrenoate (200 mg) followed by oral spironolactone (25 mg once daily) for 6 months in additi

46 day on the first postoperative day only), or spironolactone (25 mg/day).

47 2 weeks of once daily treatment with each of spironolactone (25-50 mg), bisoprolol (5-10 mg), doxazos

48 occupied by metastasis: control = 68 +/- 13, spironolactone = 26 +/- 8, P < 0.05) or inhibition of al

49 fter 21 were excluded, 285 patients received spironolactone, 282 doxazosin, 285 bisoprolol, and 274 p

50 lthy participants received the MR antagonist spironolactone (300 mg) or a placebo and underwent a str

51 sure than either bendroflumethiazide 5 mg or spironolactone 50 mg (P<0.005).

52 re traditional therapy were given amiloride, spironolactone, a combination of the two drugs, or place

53 Here we demonstrate that spironolactone, a mineralocorticoid receptor antagonist

54 Spironolactone, a nonselective mineralocorticoid recepto

55 treating severe heart failure patients with spironolactone, acceptance of this drug was overwhelming

56 Spironolactone accounted for 99.4% of MRA use.

57 Last, spironolactone acutely lowered blood pressure, which was

58 The RALES study showed that spironolactone, added to conventional therapy for chroni

59 increase in cortisol secretion levels after spironolactone administration.

60 erting-enzyme inhibitors, beta-blockers, and spironolactone) alone or in combination with cardiac-res

61 Spironolactone also modestly increased serum potassium l

62 Spironolactone also reduced the expression of osteoinduc

63 ar conditions for high-risk medications (eg, spironolactone, amiodarone).

64 To test this hypothesis, we administered spironolactone, an MR antagonist, to individuals with ma

65 0.55 [95% CI, -0.92 to -0.18] with high-dose spironolactone and -0.49 [95% CI, -0.98 to -0.14] with u

66 pg/mL among the group treated with high-dose spironolactone and 3753 (1968-7633) pg/mL among the grou

67 up, 131 patients completed therapy-64 taking spironolactone and 67 placebo.

68 Two doses each of spironolactone and bendroflumethiazide were compared.

69 -11.2%, P = 0.007) in the group assigned to spironolactone and by 16.8% (95% CI, -37.3%, +10.5%, P =

70 Cs, an effect inhibited by the MR antagonist spironolactone and by MR knock down with small interferi

71 There was a significant interaction of spironolactone and change in E/e' on VO2 (p = 0.039).

72 ence in home systolic blood pressure between spironolactone and each of the other two drugs.

73 Although steroidal antagonists such as spironolactone and eplerenone are clinically useful for

74 ineralocorticoid receptor antagonists (MRAs) spironolactone and eplerenone have proved valuable addit

75 eralocorticoid receptor antagonists, such as spironolactone and eplerenone that are used to treat sid

76 the mineralocorticoid receptor antagonists, spironolactone and eplerenone.

77 ving no or low-dose (12.5 mg or 25 mg daily) spironolactone and had NT-proBNP levels of 1000 pg/mL or

78 ar decreases in systolic blood pressure with spironolactone and HCTZ but not with placebo.

79 -EC adhesion, an effect that is inhibited by spironolactone and ICAM1 blocking antibody, supporting t

80 d from 12.7 (SD, 3.6) to 12.1 (SD, 3.7) with spironolactone and increased from 12.8 (SD, 4.4) to 13.6

81 One het group received spironolactone and lisinopril starting at 8 weeks of lif

82 Moreover, WRF (17% vs. 7% for spironolactone and placebo groups, p < 0.001) was associ

83 veraged home systolic blood pressure between spironolactone and placebo, followed (if significant) by

84 ence in home systolic blood pressure between spironolactone and the average of the other two active d

85 Physician education of the risks of spironolactone and the need for follow-up is essential.

86 The diuretics spironolactone and trichlormethiazide, but not amiloride

87 To assess the effect of high-dose spironolactone and usual care on N-terminal pro-B-type n

88 c therapy in approximately 70% and both oral spironolactone and vasodilators in approximately 90%, eu

89 alance calculation identified dexamethasone, spironolactone, and 6-alpha-methylprednisolone as major

90 before the widespread use of beta-blockers, spironolactone, and defibrillators-interventions known t

91 e treatment includes estrogens, finasteride, spironolactone, and gonadotropin-releasing hormone (GnRH

92 as they were abolished by the MR antagonist, spironolactone, and mimicked by the MR-agonist, aldoster

93 progesterone and the antihypertensive agent spironolactone, and the binding selectivity of cortisol

94 in both treatment arms, participants in the spironolactone arm had lower mortality rates at all pota

95 tion and those with WRF, particularly in the spironolactone arm, but the substantial net benefit of s

96 This study suggests Spironolactone as a new candidate for chemotherapy.

97 METHODS AND First, we identified spironolactone as a potent inhibitor of Panx1 in an unbi

98 he adequacy of monitoring patients receiving spironolactone as well as spironolactone's relationship

99 meeting enrollment criteria, 24.1% received spironolactone, as compared with 17.4% of those not meet

100 cular mechanisms of action of finerenone and spironolactone at several key steps of the MR signaling

101 s these losses, whereas its combination with spironolactone attenuates these responses to prevent bon

102 Spironolactone blocked the aldosterone-induced decrease

103 Central infusions of spironolactone blocked the increased intake of 1.8% sali

104 We found that spironolactone blunted the development of GJR and also p

105 ne or amiloride; plasma renin rose 4-fold on spironolactone but only 2-fold on bendroflumethiazide (P

106 All patients received spironolactone, but administration of all other diuretic

107 oth the AT1 receptor blocker losartan and by spironolactone, but not by aldosterone synthase inhibiti

108 In conclusion, the addition of spironolactone, but not losartan, to a regimen including

109 urrent VT/VF and who were not candidates for spironolactone by current heart failure guidelines were

110 d by the ICD and who were not candidates for spironolactone by current heart failure guidelines, spir

111 Although spironolactone can act at the mineralocorticoid receptor

112 mineralocorticoid receptor via antagonists (spironolactone, canrenoate, and eplerenone) rescues GC-i

113 +/- 759 microg/24 h, respectively), whereas spironolactone co-treatment attenuated (p < 0.05) these

114 alt and ALDO/salt + furosemide, but not with spironolactone co-treatment.

115 less hyperkalemia and more hypokalemia with spironolactone compared with non-AAs and seemed to deriv

116 , mineralocorticoid receptor antagonism with spironolactone decreased aldosterone-mediated reactive o

117 Spironolactone decreased NCC protein abundance by 66% (t

118 ft ventricular ejection fraction assigned to spironolactone did not achieve a significant reduction i

119 lactone by current heart failure guidelines, spironolactone did not delay the first recurrence of VT/

120 preserved ejection fraction, treatment with spironolactone did not significantly reduce the incidenc

121 , non-AAs were more likely to attain maximal spironolactone dose (13.9% versus 5.8%; P=0.04) and had

122 The average daily KCl and spironolactone dose was 3.3 +/- 1.5 mEq/kg and 3.5 +/- 1

123 the vascular wall with MR antagonists (i.e., spironolactone, eplerenone) may therefore account for th

124 Raptor-small interfering RNA or treated with spironolactone/eplerenone, aldosterone or pulmonary arte

125 With this report (Randomized Spironolactone Evaluation Study [RALES] trial), we noted

126 pitation assays revealed that, as opposed to spironolactone, finerenone inhibits MR, steroid receptor

127 f hyperkalemia in healthy young women taking spironolactone for acne is equivalent to the baseline ra

128 yperkalemia among healthy young women taking spironolactone for acne is unclear.

129 f hyperkalemia in healthy young women taking spironolactone for acne was calculated.

130 spective study of healthy young women taking spironolactone for acne.

131 ring is unnecessary for healthy women taking spironolactone for acne.

132 perkalemia in 974 healthy young women taking spironolactone for acne.

133 Many patients treated with spironolactone for CHF do not receive needed follow-up o

134 ropriateness and complications of the use of spironolactone for heart failure (HF) in clinical practi

135 ents, whom we identified as being started on spironolactone for HF after prerelease of the RALES tria

136 To investigate the use of spironolactone for HF in a clinical setting, we analyzed

137 m, as has flutamide (250 mg) twice daily and spironolactone for more severe cases.

138 come occurred in 320 of 1722 patients in the spironolactone group (18.6%) and 351 of 1723 patients in

139 talized longer than those in the ramipril or spironolactone group (6.8+/-8.2 days vs. 5.7+/-3.2 days

140 7.8% in the ramipril group, and 25.9% in the spironolactone group (p=.95).

141 CFR improved with treatment in the spironolactone group as compared with the HCTZ group and

142 onth, mean potassium levels increased in the spironolactone group but not in the placebo group (4.54+

143 The spironolactone group showed improvement in exercise capa

144 e had a significantly lower incidence in the spironolactone group than in the placebo group (206 pati

145 tients in the placebo group, patients in the spironolactone group were extubated sooner after surgery

146 Adjusted mean changes in KCCQ for the spironolactone group were significantly better than thos

147 68.7% in the placebo group and 84.7% in the spironolactone group.

148 us did not ingest the aldosterone antagonist spironolactone had lower distal nephron H+ secretion (29

149 Spironolactone has been shown to be an effective treatme

150 Blockade of aldosterone with spironolactone has been shown to be particularly effecti

151 yocardial compliance attributed to fibrosis, spironolactone has not been shown to alter outcomes-perh

152 nonspecific aldosterone receptor antagonist, spironolactone, have limited its usefulness in the treat

153 : 1.3 to 2.6) but not in those randomized to spironolactone (hazard ratio: 1.1, 95% confidence interv

154 st (aldosterone; EC50 1.3 nM) or antagonist (spironolactone; IC50 1.6 nM), and 53 gene expression dif

155 We further revealed that Spironolactone impairs Rad51 foci formation, sensitizes

156 enzyme (ACE) inhibitors, beta-blockers, and spironolactone improve survival in patients with heart f

157 Treatment with spironolactone improved coronary microvascular function,

158 Spironolactone improves endothelial dysfunction, increas

159 Spironolactone improves outcomes in patients with advanc

160 ment with heart failure drugs lisinopril and spironolactone improves skeletal muscle pathology in Duc

161 tors, beta-blockers, diuretics, digoxin, and spironolactone in improving outcomes for patients with t

162 Potassium increased with spironolactone in non-AAs (4.29+/-0.5-4.55+/-0.49 mmol/L

163 endroflumethiazide, would be as effective as spironolactone in overcoming the Na+ retention and lower

164 end toward improvement in LS associated with spironolactone in patients enrolled in the Americas but

165 We evaluated the effects of spironolactone in patients with heart failure and a pres

166 changes and possible clinical benefits with spironolactone in patients with heart failure and preser

167 The benefits of spironolactone in patients with heart failure with eithe

168 noted a marked increase in widespread use of spironolactone in patients with HF.

169 ning renal function (WRF) on the efficacy of spironolactone in patients with severe heart failure (HF

170 alemia was less likely in patients receiving spironolactone in the Americas with no significant treat

171 entify improvement in exercise capacity with spironolactone in the subset of patients with HFpEF with

172 lated with Raptor-small interfering RNA plus spironolactone in vivo, which decreased arteriole muscul

173 receptor antagonists, such as eplerenone and spironolactone, in improving blood pressure control in p

174 d mineralocorticoid receptor (MR) antagonist spironolactone indirectly and directly target MR.

175 Spironolactone induced reverse remodeling (left ventricu

176 Next, spironolactone inhibited alpha-adrenergic vasoconstricti

177 The mineralocorticoid receptor antagonist spironolactone inhibited AngII-induced increases in NADP

178 In addition, spironolactone inhibits expression of other SM-dependent

179 l capsid antigen is highly SM dependent, and spironolactone inhibits viral capsid antigen synthesis a

180 congestive heart failure (CHF) patients with spironolactone initiation after publication of RALES.

181 Spironolactone interacted with NYHA (P<0.001).

182 Spironolactone is an effective antihypertensive drug, es

183 We tested the hypothesis that spironolactone is associated with reduced mortality also

184 These data suggest that spironolactone is being used widely in HF without consid

185 0 patients with diastolic heart failure with spironolactone is in its final phases of planning.

186 The use of spironolactone is inversely associated with fractures in

187 The antihypertensive benefit of spironolactone is not limited to patients with demonstra

188 e primary objective was to determine whether spironolactone is superior to placebo in improving diast

189 verse cardiovascular effects in CKD and that spironolactone is worthy of further study as a treatment

190 ffinity for the MR than either eplerenone or spironolactone, Ly caused no hyperkalemia.

191 The net benefits of spironolactone may be lower outside the clinical trial s

192 Although some data suggest that spironolactone might improve outcomes in these patients,

193 g intracerebroventricular infusion (10 d) of spironolactone (MR antagonist) or RU486 (GR antagonist).

194 previous systolic blood pressure response to spironolactone of > or = 20 mm Hg.

195 orgia, and there was no detectable impact of spironolactone on any outcomes.

196 rcise E/e' mediates the beneficial effect of spironolactone on exercise capacity.

197 s were randomly assigned to receive 25 mg of spironolactone once daily (n=213) or matching placebo (n

198 ension in the 10% hypomorphs is corrected by spironolactone or amiloride at doses that do not change

199 umethiazide to be less effective than either spironolactone or amiloride; plasma renin rose 4-fold on

200 t salt restriction and diuretic therapy with spironolactone or an equivalent in the first instance.

201 LDO-treated rats was partially suppressed by spironolactone or either antioxidant.

202 Spironolactone or eplerenone prevented or reversed pulmo

203 ition of the mineralocorticoid receptor with spironolactone or eplerenone, which attenuated hypoxia-i

204 ificantly higher with the addition of either spironolactone or losartan.

205 terone Antagonist (TOPCAT) and randomized to spironolactone or placebo.

206 e levels were not significantly altered with spironolactone or RU486 in either genotype.

207 hibitors or ARBs were randomized to continue spironolactone or to receive a matching placebo.

208 These effects were abrogated by spironolactone or vascular gene transfer of G6pd.

209 with or without dexamethasone (Dex), RU-486, spironolactone, or vehicle.

210 response was also significantly reduced with spironolactone (P<0.05), with Ang II responses unaltered

211 Co-treatment with spironolactone, PDTC, or NAC attenuated these molecular

212 cologic blockade of aldosterone effects with spironolactone (percentage of lung occupied by metastasi

213 eceived (1) vehicle, (2) aldosterone, or (3) spironolactone plus aldosterone.

214 ps muscles from dystrophic mice treated with spironolactone plus lisinopril (IC50 0.1 nM) compared wi

215 Secondary measures included spironolactone prescriber profiles and potassium monitor

216 We assessed spironolactone prescriptions at hospital discharge in pa

217 Spironolactone prescriptions increased markedly after th

218 In rats with aldosteronism, spironolactone preserves skeletal strength.

219 The MR antagonists BR-4628 and spironolactone prevent these alterations.

220 erone (DHT), testosterone, R1881, estradiol, spironolactone, progesterone, and cortisol resulting in

221 haracteristics and achieved study drug dose, spironolactone reduced the combined end point of death o

222 at the mineralocorticoid receptor antagonist spironolactone reduced vascular and soft tissue calcific

223 The use of spironolactone reduces left ventricular mass and improve

224 ial was designed to test the hypothesis that spironolactone reduces the incidence of VT/VF in patient

225 The increase in CFR with spironolactone remained significant after controlling fo

226 Spironolactone restored beta-catenin-N-cadherin complexi

227 Compared with placebo, the use of spironolactone resulted in significant improvements in l

228 Spironolactone reversed interstitial fibrosis, attenuate

229 + hydrochlorothiazide (RSG+HCTZ), (4) RSG + spironolactone (RSG+SPIRO), and (5) discontinuation of R

230 patients receiving spironolactone as well as spironolactone's relationship to hyperkalemia.

231 ect due, at least in part, to stimulation of spironolactone-sensitive, PIT1-dependent osteoinductive

232 In six of the 285 patients who received spironolactone, serum potassium exceeded 6.0 mmol/L on o

233 In 30 subjects, 3 months of treatment with spironolactone significantly increased FMD (2.5+/-1.7 ve

234 Spironolactone significantly increased the forearm blood

235 terone was demonstrated by the evidence that spironolactone significantly reduced blood pressure and

236 rol with no further treatment (CONT; n = 6); spironolactone (SP) alone (200 mg/kg per d, by gavage, n

237 rone (ALDOST, 0.75 microg/h) with or without spironolactone (Spi, 100 mg/kg per daily gavage) were co

238 Here, we found that spironolactone (SPIR), an FDA-approved diuretic drug wit

239 A separate group received spironolactone (Spiro), an aldosterone receptor antagoni

240 ngiotensin receptor blockers, beta-blockers, spironolactone) stratified by socioeconomic circumstance

241 The superiority of spironolactone supports a primary role of sodium retenti

242 We studied the adoption of spironolactone therapy after publication of the Randomiz

243 Spironolactone therapy in patients with congestive heart

244 The impact of spironolactone therapy on measures of cardiac structure

245 tone arm, but the substantial net benefit of spironolactone therapy remained.

246 Twelve to 18 months of spironolactone therapy was not associated with alteratio

247 rements obtained among young women receiving spironolactone therapy, yielding a hyperkalemia rate of

248 ntricular dysfunction who were randomized to spironolactone, titrated to 25 or 50 mg daily or placebo

249 sought to determine whether the addition of spironolactone to angiotensin-converting enzyme (ACE) in

250 However, in humans, the relationship of spironolactone to fractures is not known.

251 65 healthy young women taking and not taking spironolactone to obtain a profile for the baseline rate

252 The SPIronolactone to Reduce ICD Therapy (SPIRIT) trial was

253 Adding treatment with high-dose spironolactone to usual care for patients with AHF for 9

254 effects of aldosterone were reversed by both spironolactone treatment and PIT1 silencing and were mit

255 We derived propensity scores for spironolactone treatment based on 41 covariates.

256 follow-up, and increased complications with spironolactone treatment compared with the RALES trial.

257 Spironolactone treatment decreased PAI-1 immunoreactivit

258 Furthermore, a significant effect of spironolactone treatment on corticotropin secretion leve

259 Spironolactone treatment resulted in a significant incre

260 , blockade of mineralocorticoid receptors by spironolactone treatment reversibly restored the elevate

261 4%, beta-blocker uptake from 12% to 41%, and spironolactone uptake from 3% to 20%.

262 ave been raised about the appropriateness of spironolactone use in some patients with heart failure.

263 Spironolactone use increased >7-fold (3.0% to 21.3% P<0.

264 rpose of this study was to determine whether spironolactone use is associated with fractures in men w

265 Spironolactone use was also associated with a shorter du

266 After adjustment for covariates, spironolactone use was inversely associated with total f

267 tervals of having a fracture associated with spironolactone use were estimated using conditional logi

268 spironolactone (100 mg) vs placebo or 25 mg spironolactone (usual care) daily for 96 hours.

269 is an ongoing randomized controlled trial of spironolactone versus placebo for heart failure with pre

270 low [mean+/-SEM], 177+/-29% versus 95+/-20%, spironolactone versus placebo; P<0.001), with an associa

271 Peak VO2 did not significantly change with spironolactone vs placebo (from 16.3 [SD, 3.6] mL/min/kg

272 ntrol procedure) and MR-availability (400 mg spironolactone vs. placebo) in a randomized, placebo-con

273 for propensity scores, the hazard ratio for spironolactone was 1.05 (95% confidence interval, 1.00-1

274 for propensity scores, the hazard ratio for spironolactone was 1.11 (95% confidence interval, 1.02-1

275 Use of spironolactone was an independent predictor of improved

276 Compared with placebo, spironolactone was associated with a similar risk of VT/

277 preserved ejection fraction patients, use of spironolactone was associated with an improvement in HF-

278 Treatment with spironolactone was associated with increased serum creat

279 ance of potassium and creatinine, the use of spironolactone was associated with less hypokalemia and

280 When spironolactone was given with dexamethasone, it did not

281 The absolute benefit of spironolactone was greatest in patients with reduced eGF

282 The treatment benefit of spironolactone was maintained at least until potassium e

283 tive prognosis, yet the mortality benefit of spironolactone was maintained.

284 Spironolactone was not associated with alterations in ca

285 lation of HF with reduced ejection fraction, spironolactone was not associated with reduced mortality

286 ot be generalizable, and eplerenone was, but spironolactone was not, studied in mild HF.

287 Spironolactone was prescribed to 22.8% of patients with

288 Spironolactone was reported by one prospective randomize

289 reduction in home systolic blood pressure by spironolactone was superior to placebo (-8.70 mm Hg [95%

290 However, spironolactone was the more effective natriuretic agent,

291 Spironolactone was the most effective add-on drug for th

292 Spironolactone was the most effective blood pressure-low

293 lating doses of potassium chloride (KCl) and spironolactone were administered to eight subjects with

294 of potassium levels on the effectiveness of spironolactone were assessed in a landmark analysis and

295 of these populations and their responses to spironolactone were explored.

296 The aldosterone antagonist spironolactone, when used in severe heart failure, provi

297 Moreover, we showed that, in contrast to spironolactone, which activates the S810L mutant MR resp

298 ent with the aldosterone receptor antagonist spironolactone, which has been shown to diminish sudden

299 e mineralocorticoid receptor (MR) antagonist spironolactone, which significantly reduced sodium appet

300 trate that molecules structurally related to spironolactone with similar antimineralocorticoid blocki

301 used by excessive sodium retention, and that spironolactone would therefore be superior to non-diuret