PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 21106690-3 2011 In fungiform and vallate TRCs that exhibit functional ENaC currents (e.g., amiloride-sensitive Na(+) influx), insulin (5-20 nM) caused a significant increase in Na(+) influx at -80 mV (EC(50) = 7.53 nM). Amiloride 75-84 sodium channel, nonvoltage-gated 1 alpha Mus musculus 54-58 22357920-7 2012 Inhibition of epithelial Na channel (ENaC) with amiloride or benzamil abolished the flow response, suggesting involvement of ENaC in flow-regulated ET-1 synthesis. Amiloride 48-57 sodium channel, nonvoltage-gated 1 alpha Mus musculus 37-41 21106690-9 2011 Interestingly, these differences between groups were abolished when amiloride (100 muM) was added into NaCl solutions, suggesting that insulin was regulating ENaC. Amiloride 68-77 sodium channel, nonvoltage-gated 1 alpha Mus musculus 158-162 18524855-7 2008 The hypertension was probably mediated by ENaC overactivity because 1) Nedd4-2 null mice had higher expression levels of all three ENaC subunits in kidney, but not of other Na+ transporters; 2) the downregulation of ENaC function in colon was impaired; and 3) NaCl-sensitive hypertension was substantially reduced in the presence of amiloride, a specific inhibitor of ENaC. Amiloride 333-342 sodium channel, nonvoltage-gated 1 alpha Mus musculus 42-46 21178974-7 2011 Around 30% of baseline and 50% of vasopressin-induced water flow is coupled to an amiloride-sensitive, ENaC-mediated, electrogenic sodium transport, whereas the remaining flow is coupled to an amiloride-insensitive, nonelectrogenic sodium transport mediated by an unknown electroneutral transporter. Amiloride 82-91 sodium channel, nonvoltage-gated 1 alpha Mus musculus 103-107 20016101-4 2009 The direction and pharmacology of transepithelial current was consistent with Na(+) absorption by the epithelial Na(+) channel (ENaC) and was blocked by the ENaC-specific inhibitors benzamil and amiloride. Amiloride 195-204 sodium channel, nonvoltage-gated 1 alpha Mus musculus 102-126 20016101-4 2009 The direction and pharmacology of transepithelial current was consistent with Na(+) absorption by the epithelial Na(+) channel (ENaC) and was blocked by the ENaC-specific inhibitors benzamil and amiloride. Amiloride 195-204 sodium channel, nonvoltage-gated 1 alpha Mus musculus 128-132 20016101-4 2009 The direction and pharmacology of transepithelial current was consistent with Na(+) absorption by the epithelial Na(+) channel (ENaC) and was blocked by the ENaC-specific inhibitors benzamil and amiloride. Amiloride 195-204 sodium channel, nonvoltage-gated 1 alpha Mus musculus 157-161 22332421-11 2011 Dominant negative dynamin K44A transfected into CHO cells together with ENaC subunits significantly increased amiloride-sensitive current density compared to cells transfected with ENaC subunits only (control); additional transfection of cortactin in this system resulted in current density restitution back to the control level. Amiloride 110-119 sodium channel, nonvoltage-gated 1 alpha Mus musculus 72-76 19060118-6 2009 Further, recent pharmacological studies demonstrated that preventive, but not late, inhibition of increased airway Na(+) absorption with the ENaC blocker amiloride reduced morbidity and mortality in this murine model of CF lung disease. Amiloride 154-163 sodium channel, nonvoltage-gated 1 alpha Mus musculus 141-145 19060118-7 2009 These results support a critical role of ENaC in the in vivo pathogenesis of CF lung disease and suggest that amiloride may be an effective preventive therapy for CF patients. Amiloride 110-119 sodium channel, nonvoltage-gated 1 alpha Mus musculus 41-45 18849497-2 2008 However, inhalation therapy with the ENaC blocker amiloride did not have therapeutic benefits in patients with CF with established lung disease. Amiloride 50-59 sodium channel, nonvoltage-gated 1 alpha Mus musculus 37-41 18653483-3 2008 Whole-cell patch-clamp recordings from principal cells of connecting tubules (CNT) or cortical collecting ducts (CCD) demonstrated that addition of trypsin (20 microg/ml) to the bath solution increased the ENaC-mediated amiloride-sensitive whole cell current (DeltaIAmi) in the majority of cells. Amiloride 220-229 sodium channel, nonvoltage-gated 1 alpha Mus musculus 206-210 17609287-7 2007 Induction of MLPH in these cells led to a relatively modest, but statistically significant, increase in amiloride-sensitive Na+ current, suggesting the MLPH may be involved in ENaC trafficking. Amiloride 104-113 sodium channel, nonvoltage-gated 1 alpha Mus musculus 176-180 17977920-0 2008 Amiloride-sensitive NaCl taste responses are associated with genetic variation of ENaC alpha-subunit in mice. Amiloride 0-9 sodium channel, nonvoltage-gated 1 alpha Mus musculus 82-86 17977920-2 2008 ENaC activity is blocked by amiloride, which in several mammalian species also inhibits taste responses to NaCl. Amiloride 28-37 sodium channel, nonvoltage-gated 1 alpha Mus musculus 0-4 17977920-10 2008 This suggests that the R616W variation in the alphaENaC subunit affects amiloride sensitivity of the ENaC channel and provides evidence that ENaC is involved in amiloride-sensitive salt taste responses in mice. Amiloride 72-81 sodium channel, nonvoltage-gated 1 alpha Mus musculus 51-55 17977920-10 2008 This suggests that the R616W variation in the alphaENaC subunit affects amiloride sensitivity of the ENaC channel and provides evidence that ENaC is involved in amiloride-sensitive salt taste responses in mice. Amiloride 72-81 sodium channel, nonvoltage-gated 1 alpha Mus musculus 101-105 17977920-10 2008 This suggests that the R616W variation in the alphaENaC subunit affects amiloride sensitivity of the ENaC channel and provides evidence that ENaC is involved in amiloride-sensitive salt taste responses in mice. Amiloride 161-170 sodium channel, nonvoltage-gated 1 alpha Mus musculus 51-55 17977920-10 2008 This suggests that the R616W variation in the alphaENaC subunit affects amiloride sensitivity of the ENaC channel and provides evidence that ENaC is involved in amiloride-sensitive salt taste responses in mice. Amiloride 161-170 sodium channel, nonvoltage-gated 1 alpha Mus musculus 101-105 16985514-6 2006 This effect of furosemide was abolished with amiloride or benzamil blocking ENaC action. Amiloride 45-54 sodium channel, nonvoltage-gated 1 alpha Mus musculus 76-80 15857902-1 2005 Amiloride-sensitive, epithelial Na(+) channel (ENaC)-mediated, active absorption of Na(+) is elevated in the airway epithelium of cystic fibrosis (CF) patients, resulting in excess fluid removal from the airway lumen. Amiloride 0-9 sodium channel, nonvoltage-gated 1 alpha Mus musculus 47-51 16207792-10 2006 Amiloride, ENaC-selective amiloride analogs (benzamil and phenamil), and protease inhibitors (aprotinin and leupeptin) attenuated heightened V(te) and I(sc). Amiloride 26-35 sodium channel, nonvoltage-gated 1 alpha Mus musculus 11-15 15914781-5 2005 Then, we determined pressure- and agonist-induced constriction and changes in vascular smooth muscle cytosolic Ca(2+) and Na(+) in isolated mouse renal interlobar arteries following DEG/ENaC inhibition with amiloride and benzamil. Amiloride 207-216 sodium channel, nonvoltage-gated 1 alpha Mus musculus 186-190 15914781-8 2005 Selective DEG/ENaC inhibition, with low doses of amiloride and benzamil, abolishes pressure-induced constriction and increases in cytosolic Ca(2+) and Na(+) without diminishing agonist-induced responses in isolated mouse interlobar arteries. Amiloride 49-58 sodium channel, nonvoltage-gated 1 alpha Mus musculus 14-18 15522985-1 2005 Amiloride-sensitive sodium entry, via the epithelial sodium channel (ENaC), is the rate-limiting step for Na+ absorption in kidney collecting ducts, and epidermal growth factor (EGF) inhibits Na+ transport and ENaC expression. Amiloride 0-9 sodium channel, nonvoltage-gated 1 alpha Mus musculus 69-73 15522985-1 2005 Amiloride-sensitive sodium entry, via the epithelial sodium channel (ENaC), is the rate-limiting step for Na+ absorption in kidney collecting ducts, and epidermal growth factor (EGF) inhibits Na+ transport and ENaC expression. Amiloride 0-9 sodium channel, nonvoltage-gated 1 alpha Mus musculus 210-214 12386156-6 2002 Oocytes co-injected with both G551D-CFTR and ENaC expressed an amiloride-sensitive whole cell current that was similar to that observed before and after G551D-CFTR activation with forskolin/isobutylmethylxanthine. Amiloride 63-72 sodium channel, nonvoltage-gated 1 alpha Mus musculus 45-49 15047694-6 2004 Oocytes co-injected with both CFTR and mENaC or hENaC expressed an amiloride-sensitive whole cell current that was decreased compared with that observed with the injection of mENaC or hENaC alone before CFTR activation with forskolin/3-isobutyl-1-methylxanthine. Amiloride 67-76 sodium channel, nonvoltage-gated 1 alpha Mus musculus 39-44 8589728-4 1996 The adult lung expresses alpha, beta and gamma ENaC (3,4), and an amiloride-sensitive electrogenic sodium reabsorption has been documented in upper and lower airways (3-7), but it is not established whether this sodium transport is mediated by ENaC in vivo. Amiloride 66-75 sodium channel, nonvoltage-gated 1 alpha Mus musculus 244-248 12435797-5 2002 In cultured mouse mpkCCD(cl4) principal cells, 17OHP and 20OHP also prevented the aldosterone-stimulated amiloride-sensitive component of the short-circuit current (Ams I(sc)), reflecting Na(+) absorption mediated by the epithelial Na(+) channel (ENaC). Amiloride 105-114 sodium channel, nonvoltage-gated 1 alpha Mus musculus 221-245 12435797-5 2002 In cultured mouse mpkCCD(cl4) principal cells, 17OHP and 20OHP also prevented the aldosterone-stimulated amiloride-sensitive component of the short-circuit current (Ams I(sc)), reflecting Na(+) absorption mediated by the epithelial Na(+) channel (ENaC). Amiloride 105-114 sodium channel, nonvoltage-gated 1 alpha Mus musculus 247-251 11006079-2 2000 The amiloride sensitivity of the basal current of the cultured endometrial epithelia was found to vary with the magnitude of the basal current, the higher the basal current the greater its sensitivity to amiloride, indicating possible elevation of ENaC expression. Amiloride 4-13 sodium channel, nonvoltage-gated 1 alpha Mus musculus 248-252 11006079-3 2000 However, the magnitude of the forskolin-induced Isc, previously demonstrated to be mediated by CFTR, decreased as the amiloride sensitivity of the basal current increased, suggesting a possible inhibitory effect of elevated expression of ENaC on CFTR-mediated Cl(-) secretion. Amiloride 118-127 sodium channel, nonvoltage-gated 1 alpha Mus musculus 238-242 10092651-1 1999 We previously raised an antibody (RA6.3) by an antiidiotypic approach which was designed to be directed against an amiloride binding domain on the epithelial Na+ channel (ENaC). Amiloride 115-124 sodium channel, nonvoltage-gated 1 alpha Mus musculus 171-175 10092651-4 1999 RA6.3 specifically recognized an amiloride binding domain within the alpha-subunit of mouse and bovine ENaC. Amiloride 33-42 sodium channel, nonvoltage-gated 1 alpha Mus musculus 103-107 10092651-8 1999 Selected residues docked to the antibody in a manner corresponding to the ordered linear array of amino acid residues within an amiloride binding domain on the alpha-subunit of ENaC. Amiloride 128-137 sodium channel, nonvoltage-gated 1 alpha Mus musculus 177-181 12571417-6 2002 In the distal colon, electrogenic Na(+) transport (J(Na)) mediated by the epithelial Na(+) channel (ENaC) was measured 8 h after stimulation with 3.10(-9) M aldosterone in vitro as the drop in I(SC) (short circuit current) after addition of 10(-4) M amiloride. Amiloride 250-259 sodium channel, nonvoltage-gated 1 alpha Mus musculus 74-98 12571417-6 2002 In the distal colon, electrogenic Na(+) transport (J(Na)) mediated by the epithelial Na(+) channel (ENaC) was measured 8 h after stimulation with 3.10(-9) M aldosterone in vitro as the drop in I(SC) (short circuit current) after addition of 10(-4) M amiloride. Amiloride 250-259 sodium channel, nonvoltage-gated 1 alpha Mus musculus 100-104 11564291-2 2001 The present study investigated the functional role of its subunits in regulating ENaC activity, measured as amiloride sensitive short-circuit current (I(SC)), in the mouse endometrial epithelium under different culture conditions. Amiloride 108-117 sodium channel, nonvoltage-gated 1 alpha Mus musculus 81-85 11410707-4 2001 In oocytes expressing the alphaENaC splice variant, together with beta and gammaENaC subunits, amiloride-sensitive currents were less than 20% of values obtained with the wild type ENaC. Amiloride 95-104 sodium channel, nonvoltage-gated 1 alpha Mus musculus 31-35 10788432-5 2000 The forskolin/3-isobutyl-1-methylxanthine-stimulated whole-cell conductance in hCFTR-mENaC co-injected oocytes was amiloride-insensitive, indicating an inhibition of mENaC following hCFTR activation, and it was blocked by DPC (diphenylamine-2-carboxylic acid) and was DIDS (4, 4"-diisothiocyanatostilbene-2,2"-disulfonic acid)-insensitive. Amiloride 115-124 sodium channel, nonvoltage-gated 1 alpha Mus musculus 85-90 10696530-3 2000 The ENaC-mediated sodium transport is electrogenic and creates an amiloride-sensitive transepithelial potential difference (PD). Amiloride 66-75 sodium channel, nonvoltage-gated 1 alpha Mus musculus 4-8 8589728-6 1996 Amiloride-sensitive electrogenic Na+ transport was abolished in airway epithelia from alpha-ENaC(-/-) mice. Amiloride 0-9 sodium channel, nonvoltage-gated 1 alpha Mus musculus 86-96 34914636-4 2022 This was associated with a significantly lower response to the epithelial Na+ channel (ENaC) blocker amiloride, reduced ENaC activity in split-opened collecting ducts, and defective posttranslational processing of alpha and gammaENaC subunits in the knockout mice fed with Na+ deficient diet. Amiloride 101-110 sodium channel, nonvoltage-gated 1 alpha Mus musculus 63-85 34914636-4 2022 This was associated with a significantly lower response to the epithelial Na+ channel (ENaC) blocker amiloride, reduced ENaC activity in split-opened collecting ducts, and defective posttranslational processing of alpha and gammaENaC subunits in the knockout mice fed with Na+ deficient diet. Amiloride 101-110 sodium channel, nonvoltage-gated 1 alpha Mus musculus 87-91 35512853-2 2022 Inhibition of amiloride-sensitive epithelial sodium ion channel (ENaC) has now been considered as a potential therapeutic target against COPD. Amiloride 14-23 sodium channel, nonvoltage-gated 1 alpha Mus musculus 65-69 34615377-15 2021 Ankrd36 knockout mice also showed more sensitive response to ENaC inhibitor amiloride treatment. Amiloride 76-85 sodium channel, nonvoltage-gated 1 alpha Mus musculus 61-65 34143184-2 2021 Under basal dietary conditions (0.5% K), ENaC activity, measured as amiloride-sensitive currents, was high in cells at the distal end of the distal convoluted tubule (DCT) and proximal end of the connecting tubule (CNT), a region we call the early CNT (CNTe). Amiloride 68-77 sodium channel, nonvoltage-gated 1 alpha Mus musculus 41-45 34368091-10 2021 MiR-34c could restore the AFC and lung wet/dry weight ratio in the ALI animal model, and Ussing chamber assay revealed that miR-34c enhanced the amiloride-sensitive currents associated with ENaC activity in intact H441 cell monolayers. Amiloride 145-154 sodium channel, nonvoltage-gated 1 alpha Mus musculus 190-194 35569011-7 2022 In DIN and Nphs2Deltaipod mice, inhibition of ENaC by amiloride or urinary serine protease activity by aprotinin prevents sodium retention, opening up new and promising therapeutic approaches that could be translated into the treatment of nephrotic patients. Amiloride 54-63 sodium channel, nonvoltage-gated 1 alpha Mus musculus 46-50 33949206-8 2021 These outcomes support the hypothesis that exposure to hyperoxia increases GSSG, resulting in reduced lung fluid reabsorption due to inhibition of amiloride-sensitive ENaC. Amiloride 147-156 sodium channel, nonvoltage-gated 1 alpha Mus musculus 167-171 35384364-8 2022 ENaC"s contribution was assessed with the use of the specific inhibitor amiloride. Amiloride 72-81 sodium channel, nonvoltage-gated 1 alpha Mus musculus 0-4 32506040-5 2020 Patch clamp and short circuit current measurements revealed that CFH inhibited the activity of amiloride-sensitive epithelial Na+ channel (ENaC) and cation sodium (Na+) channels in mouse alveolar cells and trans-epithelial Na+ transport across human airway cells with EC50 of 125 nM and 500 nM, respectively. Amiloride 95-104 sodium channel, nonvoltage-gated 1 alpha Mus musculus 115-137 33208364-0 2020 Engineered mutant alpha-ENaC subunit mRNA delivered by lipid nanoparticles reduces amiloride currents in cystic fibrosis-based cell and mice models. Amiloride 83-92 sodium channel, nonvoltage-gated 1 alpha Mus musculus 18-28 33208364-2 2020 Airway dehydration and impaired mucociliary clearance in CF is proposed to result in tonic epithelial sodium channel (ENaC) activity, which drives amiloride-sensitive electrogenic sodium absorption. Amiloride 147-156 sodium channel, nonvoltage-gated 1 alpha Mus musculus 118-122 33208364-6 2020 We observed a significant decrease in macroscopic as well as amiloride-sensitive ENaC currents and an increase in airway surface liquid height in CF airway cells. Amiloride 61-70 sodium channel, nonvoltage-gated 1 alpha Mus musculus 81-85 33591965-9 2021 Treatment of amiloride, an ENaC inhibitor, normalizes sweat and salt excretion in corin-deficient mice. Amiloride 13-22 sodium channel, nonvoltage-gated 1 alpha Mus musculus 27-31 32506040-5 2020 Patch clamp and short circuit current measurements revealed that CFH inhibited the activity of amiloride-sensitive epithelial Na+ channel (ENaC) and cation sodium (Na+) channels in mouse alveolar cells and trans-epithelial Na+ transport across human airway cells with EC50 of 125 nM and 500 nM, respectively. Amiloride 95-104 sodium channel, nonvoltage-gated 1 alpha Mus musculus 139-143 32009028-1 2020 Epithelial sodium channel (ENaC) is an amiloride-sensitive sodium ion channel that is expressed in epithelial tissues. Amiloride 39-48 sodium channel, nonvoltage-gated 1 alpha Mus musculus 27-31 32752278-14 2020 Dose-response curves and competition with amiloride identified CDDP as a weak inhibitor of ENaC (apparent IC50 = 1 microM) that competes with amiloride for inhibition of the channel, weakening the inhibitory actions of the latter. Amiloride 42-51 sodium channel, nonvoltage-gated 1 alpha Mus musculus 91-95 32752278-14 2020 Dose-response curves and competition with amiloride identified CDDP as a weak inhibitor of ENaC (apparent IC50 = 1 microM) that competes with amiloride for inhibition of the channel, weakening the inhibitory actions of the latter. Amiloride 142-151 sodium channel, nonvoltage-gated 1 alpha Mus musculus 91-95 32752278-15 2020 Such observations are consistent with CDDP being a partial modulator of ENaC, which possibly has a binding site that overlaps with that of amiloride. Amiloride 139-148 sodium channel, nonvoltage-gated 1 alpha Mus musculus 72-76 32299681-10 2020 Consistently, the phenotype of collecting system-Kcnj10-knockout was fully abrogated by ENaC inhibition with amiloride and ameliorated by genetic inactivation of ROMK in the collecting system. Amiloride 109-118 sodium channel, nonvoltage-gated 1 alpha Mus musculus 88-92 32260115-3 2020 The diuretic drug amiloride is known to block ENaC, producing a mild natriuresis. Amiloride 18-27 sodium channel, nonvoltage-gated 1 alpha Mus musculus 46-50 31006168-3 2019 METHODS: Activation of amiloride-sensitive currents by uPA and plg were studied in Xenopus laevis oocytes expressing murine ENaC. Amiloride 23-32 sodium channel, nonvoltage-gated 1 alpha Mus musculus 124-128 32190682-4 2020 We confirmed that alpha-ENaC is one of the target genes of miR-124-5p through dual luciferase assay and Ussing chamber assay revealed that miR-124-5p inhibited amiloride-sensitive currents associated with ENaC activity in intact H441 monolayers. Amiloride 160-169 sodium channel, nonvoltage-gated 1 alpha Mus musculus 18-28 31789848-2 2020 Recent studies from mice, rats and humans have shown that the sodium retention depends on urinary serine proteases and that it can be mitigated by blockers (amiloride, triamterene) of the epithelial sodium channel ENaC. Amiloride 157-166 sodium channel, nonvoltage-gated 1 alpha Mus musculus 214-218 31006168-5 2019 RESULTS: Experiments in Xenopus laevis oocytes expressing murine ENaC confirmed proteolytic ENaC activation by a combination of plg and uPA which stimulated amiloride-sensitive currents with concomitant cleavage of the ENaC gamma-subunit at the cell surface. Amiloride 157-166 sodium channel, nonvoltage-gated 1 alpha Mus musculus 65-69 31006168-5 2019 RESULTS: Experiments in Xenopus laevis oocytes expressing murine ENaC confirmed proteolytic ENaC activation by a combination of plg and uPA which stimulated amiloride-sensitive currents with concomitant cleavage of the ENaC gamma-subunit at the cell surface. Amiloride 157-166 sodium channel, nonvoltage-gated 1 alpha Mus musculus 92-96 31006168-5 2019 RESULTS: Experiments in Xenopus laevis oocytes expressing murine ENaC confirmed proteolytic ENaC activation by a combination of plg and uPA which stimulated amiloride-sensitive currents with concomitant cleavage of the ENaC gamma-subunit at the cell surface. Amiloride 157-166 sodium channel, nonvoltage-gated 1 alpha Mus musculus 92-96 31006168-9 2019 Amiloride prevented sodium retention in nephrotic uPA-/- mice which confirmed the critical role of ENaC in sodium retention. Amiloride 0-9 sodium channel, nonvoltage-gated 1 alpha Mus musculus 99-103 30159312-9 2018 The NaCl-induced effect was blocked by the ENaC inhibitor amiloride (IC50 = 0.47 muM). Amiloride 58-67 sodium channel, nonvoltage-gated 1 alpha Mus musculus 43-47 30969802-12 2019 The hypernatremia and hypokalemia in MST3-/- mice were significantly reversed by the ENaC inhibitor amiloride, indicating that MST3-/- mice reabsorbed more Na+ through ENaC. Amiloride 100-109 sodium channel, nonvoltage-gated 1 alpha Mus musculus 85-89 30969802-12 2019 The hypernatremia and hypokalemia in MST3-/- mice were significantly reversed by the ENaC inhibitor amiloride, indicating that MST3-/- mice reabsorbed more Na+ through ENaC. Amiloride 100-109 sodium channel, nonvoltage-gated 1 alpha Mus musculus 168-172 28365586-5 2017 Patch-clamp experiments detected amiloride-sensitive Na+ currents and TPNQ-sensitive K+ currents in DCT2/CNT, suggesting the activity of ENaC and ROMK. Amiloride 33-42 sodium channel, nonvoltage-gated 1 alpha Mus musculus 137-141 29042083-4 2018 Treatment of nephrotic mice with the serine protease inhibitor aprotinin by means of subcutaneous sustained-release pellets normalized urinary serine protease activity and prevented sodium retention, as did treatment with the ENaC inhibitor amiloride. Amiloride 241-250 sodium channel, nonvoltage-gated 1 alpha Mus musculus 226-230 28862701-5 2017 Importantly, we demonstrate that the extent of kidney injury can be partially therapeutically ameliorated in mice with nephron-specific deletions of Nedd4-2 by blocking ENaC with amiloride. Amiloride 179-188 sodium channel, nonvoltage-gated 1 alpha Mus musculus 169-173 28713285-4 2017 To this end, we fed female mice either a WD or control diet and treated them with or without a very-low-dose of the ENaC-inhibitor amiloride (1 mg/kg/day) in the drinking water for 20 weeks beginning at 4 weeks of age. Amiloride 131-140 sodium channel, nonvoltage-gated 1 alpha Mus musculus 116-120 28604611-7 2017 Gene expression analyses of laser-captured specimens in ASDN suggested the presence of non-aldosterone-dependent activation of ENaC transcription in ASDN of Nedd4-2 C2 KO mice, which was abolished by amiloride treatment. Amiloride 200-209 sodium channel, nonvoltage-gated 1 alpha Mus musculus 127-131 29251736-10 2018 Amiloride (ENaC) and hydrochlorothiazide (pendrin inhibitor) equally attenuated the effect of PGE2 on sodium transport. Amiloride 0-9 sodium channel, nonvoltage-gated 1 alpha Mus musculus 11-15 28978526-6 2017 Addition of amiloride, a specific blocker of the epithelial sodium channel (ENaC), abolished basal ion transport in both inversin knockdown and control cells, indicating ENaC involvement. Amiloride 12-21 sodium channel, nonvoltage-gated 1 alpha Mus musculus 76-80 28978526-6 2017 Addition of amiloride, a specific blocker of the epithelial sodium channel (ENaC), abolished basal ion transport in both inversin knockdown and control cells, indicating ENaC involvement. Amiloride 12-21 sodium channel, nonvoltage-gated 1 alpha Mus musculus 170-174 27170740-6 2016 Whole-cell patch-clamp recordings were used to measure amiloride-sensitive ENaC currents in nephron fragments from mice maintained on different sodium diets to vary plasma aldosterone levels. Amiloride 55-64 sodium channel, nonvoltage-gated 1 alpha Mus musculus 75-79 27413200-6 2017 The activity of ENaC measured as whole cell amiloride-sensitive current (INa) in principal cells of the cortical collecting duct (CCD) was minimal under control conditions but was increased by a high-K diet to a similar extent in knockout and wild-type animals. Amiloride 44-53 sodium channel, nonvoltage-gated 1 alpha Mus musculus 16-20 26963391-18 2016 ENaC is upregulated by ACTZ treatment and its inhibition by amiloride causes significant diuresis in NCC KO and WT mice. Amiloride 60-69 sodium channel, nonvoltage-gated 1 alpha Mus musculus 0-4 26963391-11 2016 Western blot analysis demonstrated significant enhancement in ENaC expression in medulla and cortex of NCC KO and WT mice in response to ACTZ injection for 6 days, and treatment with amiloride in ACTZ-pretreated mice caused a robust increase in salt excretion in both NCC KO and WT mice. Amiloride 183-192 sodium channel, nonvoltage-gated 1 alpha Mus musculus 62-66 25391901-5 2015 We determined that nitric oxide synthase 1 (NOS1) and NOS3 contribute to shear stress-mediated NO production in the CD, that is attenuated by low doses of the ENaC inhibitors amiloride and benzamil. Amiloride 175-184 sodium channel, nonvoltage-gated 1 alpha Mus musculus 159-163 26309024-6 2015 In consequence, ENaC activity, as monitored by the amiloride-sensitive rectal potential difference (DeltaPD), was not altered even under dietary sodium restriction. Amiloride 51-60 sodium channel, nonvoltage-gated 1 alpha Mus musculus 16-20 25941340-4 2015 In untreated mice, the mean arterial pressure was higher in knockout, compared with wild-type (WT); however, treatment with amiloride, a blocker of ENaC, abolished this difference. Amiloride 124-133 sodium channel, nonvoltage-gated 1 alpha Mus musculus 148-152 25941340-10 2015 The reduced Vte in knockout was amiloride sensitive and therefore revealed an upregulation of electrogenic ENaC-mediated Na(+) reabsorption in this segment. Amiloride 32-41 sodium channel, nonvoltage-gated 1 alpha Mus musculus 107-111 24573316-11 2014 Thus, the enhanced effect of amiloride on potassium secretion in wild-type compared to knockout mice on the alkaline diet clarify a BK- alpha/beta4-mediated potassium secretory pathway in intercalated cells driven by ENaC-mediated sodium reabsorption linked to bicarbonate secretion. Amiloride 29-38 sodium channel, nonvoltage-gated 1 alpha Mus musculus 217-221 26160150-3 2015 METHODS: ENaC was expressed in Xenopus oocytes with or without additional expression of wild type SPAK, constitutively active (T233E)SPAK, WNK insensitive (T233A)SPAK or catalytically inactive (D212A)SPAK, and ENaC activity estimated from amiloride (50 microM) sensitive current (Iamil) in dual electrode voltage clamp experiments. Amiloride 239-248 sodium channel, nonvoltage-gated 1 alpha Mus musculus 9-13 24966089-8 2014 Amiloride, an epithelial Na(+) channel (ENaC) inhibitor, normalized the BP of KO mice fed HK diets, suggesting that lack of Cyp2c44 in the CD enhances ENaC activity and increases Na(+) absorption in KO mice fed HK diets. Amiloride 0-9 sodium channel, nonvoltage-gated 1 alpha Mus musculus 14-38 24966089-8 2014 Amiloride, an epithelial Na(+) channel (ENaC) inhibitor, normalized the BP of KO mice fed HK diets, suggesting that lack of Cyp2c44 in the CD enhances ENaC activity and increases Na(+) absorption in KO mice fed HK diets. Amiloride 0-9 sodium channel, nonvoltage-gated 1 alpha Mus musculus 40-44 25531136-2 2015 Clinical limitations include TZD-induced fluid retention and body weight (BW) increase, which are inhibited by amiloride, an epithelial-sodium channel (ENaC) blocker. Amiloride 111-120 sodium channel, nonvoltage-gated 1 alpha Mus musculus 152-156 24368771-5 2014 The demonstration that amiloride, an ENaC inhibitor, lowers the blood pressure of hypertensive Cyp2c44(-/-) mice identifies a role for the channel in the hypertensive phenotype of the animals. Amiloride 23-32 sodium channel, nonvoltage-gated 1 alpha Mus musculus 37-41 24303840-8 2014 F508 mice had considerably higher levels the amiloride-sensitive fractions of ENaC nasal potential difference (ENaC-NPD) than wild-type littermates and only background levels of IalphaI in their BALF. Amiloride 45-54 sodium channel, nonvoltage-gated 1 alpha Mus musculus 78-82 24303840-8 2014 F508 mice had considerably higher levels the amiloride-sensitive fractions of ENaC nasal potential difference (ENaC-NPD) than wild-type littermates and only background levels of IalphaI in their BALF. Amiloride 45-54 sodium channel, nonvoltage-gated 1 alpha Mus musculus 111-115