ライフサイエンスコーパス: amiloride

1 al adhesion marker expression with rescue by amiloride.

2 zed by the epithelial sodium channel blocker amiloride.

3 with the acid-sensitive ion channel blocker, amiloride.

4 ly reduced upon treatment with LOE908 and/or amiloride.

5 sodium current blocked by the ENaC inhibitor amiloride.

6 ch analogs would be more or less potent than amiloride.

7 esponses were not inhibited by the diuretic, amiloride.

8 by the ENaC-specific inhibitors benzamil and amiloride.

9 ransferase inhibition, EIPA, or the diuretic amiloride.

10 ormal astrocytes, and that can be blocked by amiloride.

11 r the nonselective Ca2+,Na+ channel blocker, amiloride.

12 2 through a mechanism different from that of amiloride.

13 owed a pH50 value of 6.6 and were blocked by amiloride.

14 ditive to that induced by chlorothiazide and amiloride.

15 9 mmol/L (95% CI, 0.05 to 0.33; P<0.01) with amiloride.

16 ethacin, three with eplerenone, and six with amiloride.

17 In addition, we found that the low dose of amiloride (0.5 microg kg(-1)) had no effect on the respo

18 Amiloride 1 and 5-(N,N-hexamethylene)amiloride 2 (HMA) s

19 gly, these modifications were not altered by amiloride (100 microM, an antagonist for ASICs), tetrodo

20 ted under a variety of conditions, including amiloride (100 muM) treatment and bilateral chorda tympa

21 4-Ethoxyphenethyl-substituted amiloride 12l was found to be more potent than both amil

22 2014, 145 patients were randomly assigned to amiloride, 146 to hydrochlorothiazide, and 150 to the co

23 Amiloride 1 and 5-(N,N-hexamethylene)amiloride 2 (HMA) supposedly bind in this sodium ion sit

24 oral treatment with starting doses of 10 mg amiloride, 25 mg hydrochlorothiazide, or 5 mg amiloride

25 Amiloride 40 mg was as effective as the other diuretics.

26 receive twice-daily oral treatment of either amiloride 5 mg, fluoxetine 20 mg, riluzole 50 mg, or pla

27 nd that femoral arterial injection of either amiloride (5 and 50 mug kg(-1)) or APETx2 (100 mug kg(-1

28 A higher dose of amiloride (5 microg kg(-1), i.a.) not only blocked the p

29 sal Vt and a larger Vt change in response to amiloride (a blocker of the epithelial Na(+) channel, EN

30 by removal of bath sodium and application of amiloride, a blocker of ASIC channels, whereas the non-d

31 We used amiloride, a blocker of epithelial sodium channels, to e

32 complementation by HsNHA2 was insensitive to amiloride, a characteristic inhibitor of plasma membrane

33 Amiloride, a licensed and clinically safe blocker of ASI

34 voltage-dependent and competes with that by amiloride, a pore blocker of ASICs.

35 While blockade of ASIC1 through amiloride, a potassium sparing diuretic that is currentl

36 Recent evidence suggests that amiloride, a potent and nonselective blocker of acid-sen

37 ated by the general DEG/ENaC channel blocker amiloride, a rare feature only reported for the acid-act

38 the acid-sensing ion channel (ASIC) blocker amiloride, absent in Na+-free bathing solution, and enha

39 se indomethacin, 150 mg eplerenone, or 20 mg amiloride added to constant potassium and magnesium supp

40 g-sub-1-sub-0 units, p < .004), but not with amiloride adulteration.

41 ly abrogated by a combined pretreatment with amiloride (an antagonist of acid-sensing ion channels, A

42 The demonstration that amiloride, an ENaC inhibitor, lowers the blood pressure

43 BV transcytosis was substantially reduced by amiloride, an inhibitor of macropinocytosis.

44 ide (PAN) nephropathy rat model treated with amiloride, an inhibitor of plasminogen activation, and m

45 s," whose NaCl responses were blocked by the amiloride analog benzamil, responded robustly to light s

46 Here, we demonstrate that infusion of the amiloride analog phenamil during chronic-hypoxia treatme

47 Both PcTX-1 and benzamil, an amiloride analog, caused cell cycle arrest of D54-MG cel

48 o markedly diminished by a pretreatment with amiloride and AMG8910.

49 wo antagonists revealed that the low dose of amiloride and APETx2 greatly attenuated the pressor resp

50 ; cleavage was increased by the ENaC blocker amiloride and by a mutation that decreases ENaC activity

51 hough high affinity ENaC blockers, including amiloride and derivatives, have been described, potent a

52 , while the colonic NBC is sensitive to both amiloride and DIDS.

53 with that of AtNHE1 also partially restored amiloride and EIPA but not HOE sensitivity.

54 with those of PaNHE1) exhibited even higher amiloride and EIPA sensitivity and was also HOE-sensitiv

55 Amiloride and eplerenone have similar but lower efficaci

56 Nifedipine, amiloride and ethylisopropylamiloride were ineffective.

57 experiments, putative interaction sites for amiloride and hASIC-1 have been defined.

58 de 12l was found to be more potent than both amiloride and HMA, and the shift in potency between the

59 Here we generated chimeras to "knock in" amiloride and HOE sensitivity to PaNHE1, and we thereby

60 regions within TM4 and TM10-11 contribute to amiloride and HOE sensitivity, with both regions imparti

61 eks did not differ significantly between the amiloride and hydrochlorothiazide groups, but the fall i

62 tch clamp recordings I here demonstrate that amiloride and its analogue 5-(N,N-Dimethyl)amiloride (DM

63 The crossover also included amiloride and losartan.

64 Hence, these data suggest that amiloride and other open channel blockers bind to sites

65 Both amiloride and PcTx1 inhibited the acid-induced stimulati

66 Using molecular docking software, amiloride and related molecules were docked to model str

67 partially reduced by the addition of apical amiloride and strongly reduced by basolateral bumetanide

68 of AtNHE1 partially restored sensitivity to amiloride and the related compound 5'-(N-ethyl-N-isoprop

69 ge was reduced in a dose-dependent manner by amiloride and three analogues - benzamil, 5-(N-ethyl-N-i

70 Amiloride, and to a lesser extent allopurinol but not vi

71 ist affinity, allosterism by sodium ions and amilorides, and receptor functionality was explored.

72 er, NHE1, with its commonly used inhibitors, amiloride- and benzoylguanidine (Hoechst type inhibitor

73 Although highly homologous to the amiloride- and HOE-sensitive human NHE1 (hNHE1), AtNHE1

74 TFFLF) greatly increased sensitivity to both amiloride- and HOE-type compounds, despite the fact that

75 s insensitive to HOE-type and PaNHE1 to both amiloride- and HOE-type compounds.

76 a consequence open channel blockers such as amiloride are allowed deeper into the pore providing a m

77 e response for each diuretic and to evaluate amiloride as an alternative to spironolactone.

78 eferential block of Ca(V)3.2 channels labels amiloride as the only organic blocker to be selective fo

79 hypomorphs is corrected by spironolactone or amiloride at doses that do not change blood pressure in

80 thesis, we determined in decerebrate cats if amiloride attenuated the pressor and cardioaccelerator r

81 In contrast, the high dose of amiloride attenuated the pressor responses to lactic aci

82 ironolactone and trichlormethiazide, but not amiloride, attenuated rosiglitazone effects on volume ex

83 Conversely, amiloride, benzamil and EIPA rarely blocked firing entir

84 Amiloride, benzamil and EIPA significantly decreased fir

85 copper-containing 1 (AOC1; formerly known as amiloride-binding protein 1) is a secreted glycoprotein

86 Hexamethylene amiloride binds the polar amino-terminal lumen, whereas

87 In addition, amiloride block of Ca(V)3.2 channels is mainly due to an

88 ressing human Ca(V)3 channels, we found that amiloride blocked the human Ca(V)3 channels in a concent

89 g, whereas in the presence of bumetanide and amiloride (blockers of electroneutral Na(+) movement), t

90 hibition of NHE1 with 5'-N-ethyl-N-isopropyl-amiloride blocks H/R induced apoptosis, indicating the i

91 The results demonstrate that amiloride blocks human Ca(V)3 channels differentially th

92 membrane where the sodium channel inhibitor, amiloride, blocks endocytosis and inhibits TAT transduct

93 miloride or 10microM 5-(N-methyl-N-isobutyl) amiloride, both selective inhibitors of Na(+)-H(+) excha

94 -NDI development in mice similar to thiazide/amiloride but with fewer adverse effects.

95 Consistent with previous reports, adding amiloride caused greater reductions in transepithelial v

96 tion of the Na(+)/K(+) pump (ouabain), ENaC (amiloride), CF transmembrane conductance regulator (CFTR

97 etect the compound stimulus across all MSG (+amiloride) concentrations due, in part, to the taste of

98 on.(125)I-CXCL1 endocytosis was inhibited by amiloride, cytochalasin D, and the PKC inhibitor Go6976

99 Inhibitors of MPC, Cytochalasin D and amiloride, decreased P27-mediated uptake of soluble dext

100 helial fluid transport, in part by restoring amiloride-dependent sodium transport.

101 We have identified the amiloride derivative phenamil as a stimulator of osteobl

102 hesis and evaluation of novel 5'-substituted amiloride derivatives as hA2AAR allosteric antagonists.

103 The potency of the amiloride derivatives was assessed by their ability to d

104 as inhibited by the common Orco antagonists amiloride derivatives.

105 ed to active treatment; one patient assigned amiloride died from metastatic lung cancer, one patient

106 t amiloride and its analogue 5-(N,N-Dimethyl)amiloride (DMA) block the channels at low but not at hig

107 SNP and dimethyl amiloride (DMA), an NHE inhibitor, inhibited pH(i) recov

108 on regardless of stimulus, and suggests that amiloride does not appreciably impact responses to nonso

109 Eplerenone and amiloride each increased plasma aldosterone by 3-fold an

110 CTZ, a CA inhibitor), 5-(N-Ethyl-N-isopropyl)amiloride (EIPA) (Na(+)/H(+) exchange blocker), disodium

111 nalogues - benzamil, 5-(N-ethyl-N-isopropyl) amiloride (EIPA) and hexamethyleneamiloride (HMA), reach

112 5-(N-Ethyl-N-isopropyl)amiloride (EIPA) and soluble THY-1 blocked HCMV infectio

113 the related compound 5'-(N-ethyl-N-isopropyl)amiloride (EIPA) but not to HOE694.

114 th the NHE inhibitor 5-(N-ethyl-N-isopropyl) amiloride (EIPA) resulted in a robust inhibition of LCMV

115 rthermore, 50 mum of 5-(N-ethyl-N-isopropyl)-amiloride (EIPA), a specific inhibitor for Na(+)/H(+) an

116 e by the Na(+)/H(+) exchanger ethylisopropyl amiloride (EIPA).

117 nocytosis inhibitor, 5-(N-ethyl-N-isopropyl) amiloride (EIPA).

118 lected Na(+) and Cl(-) transport inhibitors (amiloride, GlyH-101, Niflumic acid) and agonists (Forsko

119 was reported in seven (4.8%) patients in the amiloride group and three (2.3%) patients in the combina

120 nd 24 weeks, were significantly lower in the amiloride group than in the hydrochlorothiazide group (m

121 132 participants in the amiloride group, 134 in the hydrochlorothiazide group, a

122 cross study groups (ten [9%] patients in the amiloride group, seven [6%] in the fluoxetine group, 12

123 entration was 5.8 mmol/L in a patient in the amiloride group.

124 ed first between the hydrochlorothiazide and amiloride groups, and then between the hydrochlorothiazi

125 Amiloride has been reported to selectively kill human ma

126 Although amiloride has been shown to antagonize ASICs, it also ha

127 At cytotoxic concentrations, amiloride has multiple drug targets including inhibition

128 te injury in the PAN nephropathy model, with amiloride having podocyte-protective properties.

129 e the functional properties of hexamethylene amiloride (HMA)-derived compounds that inhibit the wild-

130 ith an NHE1 inhibitor, 5-(N,N-hexamethylene) amiloride (HMA).

131 omized, open-label crossover trial comparing amiloride/hydrochlorothiazide (5 mg/50 mg daily) with di

132 ved in some T1R1 and T1R3 KO mice when MSG + amiloride + IMP was tested suggests that a T1R1 or T1R3

133 MP alone, yet some were able to detect MSG + amiloride + IMP, but only at the higher MSG concentratio

134 nt with the epithelial Na(+) channel blocker amiloride, improving airway surface hydration and mucus

135 ond, we tested the neuroprotective effect of amiloride in a cohort of 14 patients with primary progre

136 rolled trials measuring neuroprotection with amiloride in patients with multiple sclerosis.

137 dy, we tested the neuroprotective effects of amiloride in patients with primary progressive multiple

138 mpletely abolished after a pretreatment with amiloride in TRPV1(-/-) mice.

139 SIC-like inward currents (blocked by 100 muM amiloride) in approximately 40% of NTS neurons, while at

140 Amiloride, in contrast, abolished PC2 currents in both t

141 hium-NDI mice with acetazolamide or thiazide/amiloride induced similar antidiuresis and increased uri

142 introduction of uPA shRNA in tumor cells or amiloride-induced uPA inhibition reduced tumorigenesis i

143 The ENaC channel blocker amiloride inhibited MSHA, whereas other inhibitors of st

144 ereas in Ca(V)3.1 and Ca(V)3.3 channels, the amiloride inhibition is equally effective from both side

145 tosis through the uptake of FITC-dextran and amiloride inhibition of Francisella LVS uptake.

146 Accordingly, amiloride injection into the NTS reduced phrenic nerve a

147 s, whereas the non-desensitizing current was amiloride insensitive and voltage dependent.

148 hways underlying salty taste in mammals, the amiloride-insensitive (AI) pathway is the least understo

149 Responses in the amiloride-insensitive (AI) pathway, one of the two pathw

150 sed responses of amiloride-sensitive but not amiloride-insensitive cells.

151 hat the Ca(v)2 homolog, Dmca1A, mediated the amiloride-insensitive component of LVA current.

152 but not NKAIN1, induces voltage-independent amiloride-insensitive Na(+)-specific conductance that ca

153 colon, while NBCe1B/C encodes electrogenic, amiloride-insensitive Na-HCO3 cotransport in proximal co

154 Ion substitutions revealed that amiloride-insensitive NaCl responses depended on Cl(-) r

155 trate that Cl(-), not Na(+), generates these amiloride-insensitive salt taste responses.

156 a key determinant of taste transduction for amiloride-insensitive salt taste.SIGNIFICANCE STATEMENT

157 Functional analyses revealed that amiloride-insensitive, electrogenic, pH gradient-depende

158 ant because much of human salt taste also is amiloride-insensitive.

159 Because amiloride is a potent inhibitor of the epithelial sodium

160 Amiloride is a small molecule diuretic, which has been u

161 ation in multiple sclerosis and suggest that amiloride may exert neuroprotective effects in patients

162 These findings suggest that amiloride may modulate seizure generation and propagatio

163 NHE1-specific inhibitor N-Methyl-N-isobutyl Amiloride (MIA) dramatically disrupted branching morphog

164 , 2016, 445 patients were randomly allocated amiloride (n=111), fluoxetine (n=111), riluzole (n=111),

165 sis included 393 patients who were allocated amiloride (n=99), fluoxetine (n=96), riluzole (n=99), an

166 observed to elevated cAMP in the presence of amiloride nor to bumetanide, a blocker of Na(+),K(+),2Cl

167 her determined and quantified the effects of amiloride on the occurrence of limbic seizures and statu

168 s were insensitive to 10 muM ethyl-isopropyl amiloride or 100 muM 4,4'- diisothiocyanatostilbene-2,2'

169 nhibited by 10microM 5-(N-ethyl-N-isopropyl) amiloride or 10microM 5-(N-methyl-N-isobutyl) amiloride,

170 ange (luminal 10 mum 5-(N-ethyl-N-isopropyl) amiloride or 25 mum HOE694) slows restitution 72-83% in

171 selective inhibitors of NHE1 and NCX1.1 than amiloride or DCB, respectively.

172 c acidification because inhibition of NHE by amiloride or lithium under physiological or weak bufferi

173 Inhibition of macropinocytosis with either amiloride or wortmannin blocked the increase in macropin

174 allopurinol), a Na(+)/H(+) exchange blocker (amiloride), or an oxygen free radical scavenger (vitamin

175 inocytosis inhibitor, 5-(N-ethyl-N-isopropyl)amiloride, or Rab5/Rab4 depletion with small interfering

176 less effective than either spironolactone or amiloride; plasma renin rose 4-fold on spironolactone bu

177 miloride, 25 mg hydrochlorothiazide, or 5 mg amiloride plus 12.5 mg hydrochlorothiazide; all doses we

178 r the combination, support first-line use of amiloride plus hydrochlorothiazide in hypertensive patie

179 dia or blocking natural sodium channels with amiloride prevents this effect.

180 on-CF epithelia, the Na(+) channel inhibitor amiloride produced similar reductions in Gt and Na(+) ab

181 er, blocking acid-sensing ion channel 1 with amiloride protected both myelin and neurons from damage

182 sm of block, and to obtain insights into the amiloride putative binding sites in Ca(V)3 channels.

183 While amiloride reduces pH(i) of malignant gliomas by inhibiti

184 tunities for probing the proton, Ca(2+), and amiloride regulation of DEG/ENaC channels and insight in

185 whereas the inhibitory effect of low pH and amiloride remained intact.

186 Inhibition of ENaC by amiloride reproduced alveolar fluid and Cl(-) secretion

187 Basal NPD was significantly associated with amiloride-resistant but not ENaC fraction.

188 Amiloride's glioma cytotoxicity can be explained, at lea

189 ted by prepulses to -50 mV and was partially amiloride sensitive.

190 I: -6.03 to -4.52, P < 0.00001, I(2) = 42%), amiloride-sensitive (ENaC) (-2.87 mV, 95% CI: -4.02 to -

191 One is the amiloride-sensitive acid-sensing sodium channel (ASIC3),

192 tion of 8-pCPT-cGMP in BALB/c mice increased amiloride-sensitive alveolar fluid clearance by approxim

193 eversibly activates human ENaC (hENaC) in an amiloride-sensitive and dose-dependent manner in heterol

194 thelial potential difference, an increase of amiloride-sensitive apical Na(+) absorption, a defective

195 In polarized M1 cells, 14,15-EET inhibited amiloride-sensitive apical to basolateral sodium transpo

196 that AR significantly increased responses of amiloride-sensitive but not amiloride-insensitive cells.

197 ENaC subunits may underlie the diversity of amiloride-sensitive cation conductances observed in a wi

198 aracteristically displaying a basally active amiloride-sensitive cation current not seen in normal hu

199 Altogether, AR increased responses of amiloride-sensitive cells required ENaCalpha and ENaCdel

200 through a mechanism that increases CFTR and amiloride-sensitive channel function.

201 on channels (ASICs) are voltage-independent, amiloride-sensitive channels involved in diverse physiol

202 Amiloride-sensitive current and ENaC abundance rose with

203 AP301 can increase amiloride-sensitive current in A549 cells as well as in

204 by assessing the effects of P2R agonists on amiloride-sensitive current in the rat CD.

205 pressing human alpha-, beta-, and gammaENaC, amiloride-sensitive current was altered by protons in th

206 siRNA inhibited the constitutively activated amiloride-sensitive current, decreased migration, and in

207 ession of ENaC in CCD cells, down-regulating amiloride-sensitive current.

208 ith SPX-101 causes a significant decrease in amiloride-sensitive current.

209 o Cl(2) (0-500 ppm for 30 min) and Na(+) and amiloride-sensitive currents (I(Na) and I(amil), respect

210 ce; GFP+) had significantly lower whole-cell amiloride-sensitive currents and single channel activity

211 protein, decreases ENaC membrane levels and amiloride-sensitive currents in both Xenopus oocytes, in

212 0W completely reversed the RSV inhibition of amiloride-sensitive currents in GFP+ cells.

213 proteolytic processing of the alpha subunit, amiloride-sensitive currents in oocytes expressing chann

214 ed whether channels of the epithelial sodium/amiloride-sensitive degenerin (ENaC/DEG) family are a ma

215 ons resulted in similar twofold increases in amiloride-sensitive ENaC current.

216 Changes in amiloride-sensitive epithelial Na(+) channel (ENaC) acti

217 that passive apical uptake of sodium via the amiloride-sensitive epithelial Na(+) channel (ENaC) and

218 s to show how and why overstimulation of the amiloride-sensitive epithelial Na(+) channel (ENaC) expr

219 embrane conductance regulator (CFTR) and the amiloride-sensitive epithelial Na(+) channel (ENaC).

220 nel 1 (ASIC1) is a H(+)-gated channel of the amiloride-sensitive epithelial Na(+) channel (ENaC)/dege

221 clearance (AFC) in vivo and the activity of amiloride-sensitive epithelial Na(+) channels (ENaC) by

222 2 (encoded by the Nedd4L gene) regulates the amiloride-sensitive epithelial Na+ channel (ENaC/SCNN1)

223 he cellular mechanisms by which RSV inhibits amiloride-sensitive epithelial Na+ channels (ENaC), the

224 caused by loss-of-function mutations of the amiloride-sensitive epithelial sodium channel (ENaC) and

225 electrogenic sodium reabsorption through the amiloride-sensitive epithelial sodium channel (ENaC).

226 Amiloride-sensitive epithelial sodium channels (ENaC) pl

227 uses decrease the expression and function of amiloride-sensitive epithelial sodium channels (ENaCs) h

228 ) demonstrated that A2BAR signaling enhanced amiloride-sensitive fluid transport and elevation of pul

229 of 1 ng/ml trypsin for 60 min stimulated the amiloride-sensitive human ENaC conductance (g(Na)) by ap

230 Amiloride-sensitive ion channels are formed from homo- o

231 lumes are coupled to dexamethasone dependent amiloride-sensitive ion transport.

232 ype I cells may detect sodium (Na(+)) via an amiloride-sensitive mechanism, suggesting they play a ro

233 but did not increase apical membrane ENaC or amiloride-sensitive Na current (I(sc)).

234 -clamp recordings reveal that TRP family and amiloride-sensitive Na(+) channels mediate touch-evoked

235 The effects of H(2)O(2) on ENaC P(o) and amiloride-sensitive Na(+) current were abolished by inhi

236 f these mice demonstrates markedly increased amiloride-sensitive Na(+) flux compared with wild-type l

237 MP-activated protein kinase (AMPK) inhibited amiloride-sensitive Na(+) transport across human H441 ep

238 associated with macropinocytosis, including amiloride-sensitive Na(+)/H(+) exchange, protein kinase

239 eins (DEG/ENaCs) that form nonvoltage-gated, amiloride-sensitive Na+ channels.

240 00W (1 microM) resulted in a doubling of the amiloride-sensitive Na+ current in GFP+ cells.

241 onclude from these data that electroneutral, amiloride-sensitive NBC is encoded by NBCn1C/D and is pr

242 hree subunits of the aldosterone-responsive, amiloride-sensitive nonvoltage-gated sodium channel enco

243 d that DmalphaG (Ca(v)3 homolog) encoded the amiloride-sensitive portion of the transient LVA calcium

244 rned performance was dependent on input from amiloride-sensitive receptors likely in the palate.

245 or low-salt diet had a significantly higher amiloride-sensitive rectal potential difference (PDamil)

246 of taste cells and that these cells mediate amiloride-sensitive salty taste.

247 8-pCPT-cGMP increased amiloride-sensitive short-circuit current (I(sc)) across

248 The increase in the amiloride-sensitive short-circuit current in Clcn2(-/-)

249 e EDC or LDC of Clcn2(-/-) mice, whereas the amiloride-sensitive short-circuit current was increased

250 dehyde caused a dose-dependent inhibition of amiloride-sensitive short-circuit Na(+) currents in H441

251 ion channels including degenerin/epithelial amiloride-sensitive sodium (DEG/ENaC) channels has been

252 masome inhibitors and notably, inhibition of amiloride-sensitive sodium (Na(+)) channels.

253 calbindin, GC1alpha2, GC1beta2, PDE5, PDE2A, amiloride-sensitive sodium channel ACCN4, and CatSper1.

254 to orbital shaking resulted in a decrease of amiloride-sensitive sodium current by approximately 60%

255 tion after aldosterone stimulation increased amiloride-sensitive sodium transport and sensitivity to

256 )CCD(14) cells resulted in a slow decline in amiloride-sensitive sodium transport with short circuit

257 DNA damage did not increase levels of the amiloride-sensitive sodium-hydrogen exchanger isoform 1

258 Insulin significantly augmented amiloride-sensitive transepithelial flux in these cells.

259 Like human CF, CFTR(/) pigs showed increased amiloride-sensitive voltage and current, but lack of api

260 ability hyperpolarises Vt and also increases amiloride-sensitive Vt, these effects are too small to a

261 age and an approximately 10-fold decrease in amiloride-sensitive whole cell conductance as compared w

262 xpression and a significant reduction in the amiloride-sensitive whole cell current as compared with

263 t not 8-Br-cGMP (a PKGI activator) increased amiloride-sensitive whole cell currents in H441 cells in

264 C43A,C557A mutant had significantly reduced amiloride-sensitive whole cell currents, enhanced Na(+)

265 In contrast, amiloride-sensitive, electroneutral, [H(+)]-dependent NB

266 15 exhibited an 80% and 91% reduction in the amiloride-sensitive, whole-cell conductance in high and

267 Gain of amiloride sensitivity appeared to correlate with increas

268 ous doses (5, 10, 30, 100, and 200 mg/kg) of amiloride significantly delayed the onset of the first e

269 d by warming, and exposure to bumetanide and amiloride slows the temperature-dependent amplitude decl

270 hange blocker and micropinocytosis inhibitor amiloride, suggesting that PepB2 invokes macropinocytosi

271 At the dose of 100 and 200 mg/kg, amiloride suppressed limbic seizures in 33% of pilocarpi

272 with the ion channel inhibitor hexamethylene amiloride than were the more crippled parental viruses w

273 itated sperm using either the ENaC inhibitor amiloride, the CFTR agonist genistein or the K(+) ionoph

274 Like amiloride, the combination of Cariporide and SEA0400 pro

275 Remarkably, amiloride then demonstrated good clinical efficacy in a

276 with RHTN, and addition of spironolactone or amiloride to the standard 3-drug antihypertensive regime

277 is differential block of Ca(V)3 channels by amiloride, to establish the mechanism of block, and to o

278 ubstitution of a potassium-sparing diuretic, amiloride, to treatment with a thiazide can prevent gluc

279 Thiazide/amiloride-treated mice showed hyponatremia, hyperkalemia

280 Oral amiloride treatment dropped performance to virtually cha

281 reatment phase) and during (treatment phase) amiloride treatment for a period of 3 years.

282 We also tested the effects of amiloride treatment on tissue damage in the mouse models

283 oth ML and PCL in CF, and greatly reduced by amiloride treatment or mucin washout.

284 Application of LOE-908 and amiloride, TRPC and TRPP2 channel blockers, respectively

285 5-Benzylglycinyl-amiloride (UCD38B) is the parent molecule of a class of

286 Our data suggest the low dose of amiloride used in our experiments selectively blocked AS

287 en any active treatment and placebo in PBVC (amiloride vs placebo, 0.0% [95% CI -0.4 to 0.5; p=0.99];

288 nflux inhibitors ranolazine, furosemide, and amiloride was evaluated.

289 Amiloride was protective against PAN-induced glomerular

290 Amiloride was shown to block cortical spreading depressi

291 Amiloride was the first organic blocker to selectively b

292 Uptake was inhibited by amiloride, whereas marginally affected by filipin and ca

293 of the allosteric effects of sodium ions and amiloride, whereas orthosteric ligand binding was decrea

294 tively responsive to sodium and inhibited by amiloride, whereas the aversive one functions as a non-s

295 t component of depolarization was blocked by amiloride, whereas the sustained component was eliminate

296 polar disorder are treated with thiazide and amiloride, which are thought to induce antidiuresis by a

297 ells that respond to NaCl in the presence of amiloride, which is significant because much of human sa

298 This work examines the interaction of amiloride with acid-sensing ion channel-1, a protein who

299 The combination of amiloride with hydrochlorothiazide, at doses equipotent

300 2.50) mutation also decreased the potency of amiloride with respect to ligand displacement but did no