| Name | NPPB |
|---|---|
| Synonyms | BNP; BNP 32; Brain natriuretic peptide; Brain natriuretic peptide 32; Gamma brain natriuretic peptide; NPPB; Natriuretic peptide precursor B; Natriuretic peptides B… |
| Name | diphenylamine |
|---|---|
| CAS |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 1375640 | Sun XP, Supplisson S, Torres R, Sachs G, Mayer E: Characterization of large-conductance channels in rabbit colonic smooth muscle. J Physiol. 1992 Mar;448:355-82. The stilbene derivative diiso-thiocyanato-stilbene-disulphonic acid (DIDS) and the diphenylamine-2-carboxylate analogue 5-nitro-2-(3-phenylpropylamino)- (NPPB) caused a dose-dependent, reversible flicker block of the small conductance and significantly reduced the macroscopic current flow through the channel. 6. |
81(1,1,1,1) | Details |
| 1284079 | Kubo M, Okada Y: Volume-regulatory Cl- channel currents in cultured human epithelial cells. . J Physiol. 1992 Oct;456:351-71. The outward and inward currents were equally inhibited by a carboxylate analogue Cl- channel blocker, 5-nitro-2-(3-phenylpropylamino)- (NPPB) or diphenylamine-2-carboxylate (DPC) at higher doses (IC50 = 25 for NPPB or 350 microM for DPC). |
81(1,1,1,1) | Details |
| 11275682 | Lionetto MG, Giordona ME, Nicolardi G, Schettino T: Hypertonicity stimulates Cl (-) transport in the intestine of fresh water acclimated eel, Anguilla anguilla. Cell Physiol Biochem. 2001;11(1):41-54. This last phase is inhibited by drugs known to block Cl (-) absorption in eel intestine, such as luminal bumetanide (10 microM), specific inhibitor of Na (+)-K (+)-2Cl (-) cotransport, or basolateral NPPB (0.5 mM), dichloro-DPC (0.5 mM), inhibitors of basolateral Cl (-) conductance. |
1(0,0,0,1) | Details |
| 7838687 | Komwatana P, Dinudom A, Young JA, Cook DI: Characterization of the Cl- conductance in the granular duct cells of mouse mandibular glands. Pflugers Arch. 1994 Oct;428(5-6):641-7. Finally, we show that the conductance is not blocked by the addition of any of the following compounds to the extracellular solution: anthracene-9-carboxylate (A9C, 1 mmol/l), diphenylamine-2-carboxylate (DPC, 1 mmol/l), 5-nitro-2-(3-phenylpropylamino)- (NPPB, 100 mumol/l), 4,4'-diisothiocyanato-stilbene-2,2'-disulphonate (DIDS, 100 mumol/l), indanyloxyacetic acid (IAA-94, 100 mumol/l), (100 mumol/l), glibenclamide (100 mumol/l) and Ba2+ (5 mmol/l). |
0(0,0,0,0) | Details |
| 8776414 | Zhang J, Lieberman M: conductance is activated by membrane distention of cultured chick heart cells. Cardiovasc Res. 1996 Jul;32(1):168-79. The induced currents were inhibited by Cl- channel blockers, diphenylamine-2-carboxylate (DPC) and 5-nitro-2-(3-phenylpropylamino)- (NPPB), and were almost completely suppressed by gadolinium. |
81(1,1,1,1) | Details |
| 10516274 | Yanagawa N, Pham C, Shih RN, Miao S, Jo OD: dependency of renal brush-border membrane transport. . Am J Physiol. 1999 Oct;277(4 Pt 2):F506-12. It was found that the Na (+)-dependent BBM (32) P uptake was significantly inhibited by Cl (-) replacement in the uptake solution with other anions, or by Cl (-) transport inhibitors, including DIDS, SITS, diphenylamine-2-carboxylate (DPC), niflumic acid (NF), and 5-nitro-2-(3-phenylpropylamino) (NPPB). |
81(1,1,1,1) | Details |
| 8762062 | Brown CD, Dudley AJ: Chloride channel blockers decrease intracellular pH in cultured renal epithelial LLC-PK1 cells. Br J Pharmacol. 1996 Jun;118(3):443-4. A significant intracellular acidification was found with addition of 100 microM 5-nitro-2-(3-phenylpropylamino)- (NPPB), niflumic acid, flufenamate and diphenylamine-2-carboxylate (DPC) but not with 4,4'-diisothiocyanatostilbene-2-2'disulphonic acid (DIDS). |
0(0,0,0,0) | Details |
| 8392563 | Petersen KU, Cormann P, Macherey HJ, Sprakties G, Winterhager JM: Electrogenic and electroneutral HCO3-secretion by guinea pig gallbladder epithelium: discriminatory abilities of Cl- channel blockers. J Pharmacol Exp Ther. 1993 Jul;266(1):65-73. With one exception, effective agents (concentration range 10 (-5)-10 (-4) M, luminal bath) including NPPB and diphenylamine-carboxylic acid inhibited secretory HCO3- fluxes in the presence and absence of PGE1 as well as PGE1-induced Isc. |
38(0,1,2,3) | Details |
| 2546446 | Isozaki T, Yoshitomi K, Imai M: Effects of Cl- transport inhibitors on Cl- permeability across hamster ascending thin limb. Am J Physiol. 1989 Jul;257(1 Pt 2):F92-8. To characterize the mechanism of the Cl- conductance across the ATL, we examined effects on Cl- permeability across hamster ATL of Cl- transport inhibitors, including 5-nitro-2-(3-phenylpropylamino)- (NPPB), diphenylamine carboxylate (DPC), and anthracene-9-carboxylic acid (9-AC), by the in vitro microperfusion technique. |
36(0,1,1,6) | Details |
| 1320252 | Wu G, Hamill OP: NPPB block of Ca (++)-activated Cl- currents in Xenopus oocytes. Pflugers Arch. 1992 Feb;420(2):227-9. NPPB (5-nitro-2-(3-phenylpropylamino)- a member of the novel class of Cl- channel blockers related to diphenylamine-2-carboxylate, was studied for its effect on the Ca (++)-activated Cl- current (ICl (Ca)) in frog (Xenopus laevis) oocytes. |
35(0,1,1,5) | Details |
| 19176889 | Avella M, Ducoudret O, Pisani DF, Poujeol P: Swelling-activated transport of in cultured gill cells of sea bass: physiological adaptation and pavement cell plasticity. Am J Physiol Regul Integr Comp Physiol. 2009 Apr;296(4):R1149-60. Epub 2009 Jan 28. This transport was reduced by various anion channel inhibitors with the following efficiency: 5-nitro-2-(3-phenylpropylamino) (NPPB) > niflumic acid > DIDS = diphenylamine-2-carboxylic acid. |
32(0,1,1,2) | Details |
| 1696431 | Venglarik CJ, Bridges RJ, Frizzell RA: A simple assay for agonist-regulated Cl and K conductances in salt-secreting epithelial cells. Am J Physiol. 1990 Aug;259(2 Pt 1):C358-64. Forskolin- and ionomycin-stimulated I effluxes were inhibited by the Cl-channel blockers diphenylamine-2-dicarboxylate (DPC), 5-nitro-2-(3-phenylpropyl-amino) (NPPB), and 2-[cyclopentyl-6,7-dichloro-2,3-dihydro-2-methyl-1-oxo-1H- inden-5-yl) oxy] (IAA-94) and by high external K. |
31(0,1,1,1) | Details |
| 7505652 | Popp R, Englert HC, Lang HJ, Gogelein H: Inhibitors of nonselective cation channels in cells of the blood-brain barrier. EXS. 1993;66:213-8. Like the nonselective cation channel of rat exocrine pancreatic cells, the channel in cerebral capillary endothelial cells was inhibited reversibly by derivatives of diphenylamine-2-carboxylate (DPC), like 3',5-dichlorodiphenylamine-2-carboxylic acid (DCDPC, ki = 1 microM), and flufenamic acid (ki = 4.9 microM). 4'-methyldiphenylamine-2-carboxylic acid (4-MDPC), 5-chloro-2 (3-trifluormethylphenylamino)-3-nitrobenzoic acid, and 5-nitro-2-(3-phenylpropylamino)-2-carboxylic acid (NPPB), as well as the antiinflammatory drug ((Z)-5-chloro2,3-dihydro-3--2-thienylmethylene)-2-ox o-1H--1- carboxamide (Tenidap)) had a relatively low blocking potency (ki > 10 microM). |
31(0,1,1,1) | Details |
| 9426299 | Krick W, Dolle A, Hagos Y, Burckhardt G: Characterization of the conductance in porcine renal brush-border membrane vesicles. Pflugers Arch. 1998 Feb;435(3):415-21. Conductive Cl- flux had a low activation energy and was inhibited by suphhydryl reagents, the stilbene disulphonates 4-acetamido-4'-isothiocyanatostilbene-2,2'-disulphonate (SITS) and 4, 4'-diisothiocyanato-2,2'-disulphonate (DIDS), and the arylaminobenzoates diphenylamine-2-carboxylic acid (DPC) and 5-nitro-2-(3-phenylpropylamino) (NPPB). |
31(0,1,1,1) | Details |
| 11171361 | Land SC, Collett A: Detection of Cl- flux in the apical microenvironment of cultured foetal distal lung epithelial cells. J Exp Biol. 2001 Feb;204(Pt 4):785-95. In all cases, 50-70 % of J (Cl) was abolished by Cl- channel blockade using 10 micromol x l (-1) diphenylamine-2-carboxylic acid (DPC) or 5-nitro-2-(3-phenylpropylamino) (NPPB). |
31(0,1,1,1) | Details |
| 9486141 | Furukawa T, Ogura T, Katayama Y, Hiraoka M: Characteristics of rabbit ClC-2 current expressed in Xenopus oocytes and its contribution to volume regulation. Am J Physiol. 1998 Feb;274(2 Pt 1):C500-12. ClC-2 currents were inhibited by 5-nitro-2-(3-phenylpropylamino) (NPPB), diphenylamine-2-carboxylic acid (DPC), and anthracene-9-carboxylic acid (9-AC), with a potency order of NPPB > DPC = 9-AC, but were resistant to stilbene disulfonates. |
31(0,1,1,1) | Details |
| 1372482 | Cunningham SA, Worrell RT, Benos DJ, Frizzell RA: cAMP-stimulated ion currents in Xenopus oocytes expressing CFTR cRNA. Am J Physiol. 1992 Mar;262(3 Pt 1):C783-8. In addition, the Cl channel blockers 5-nitro-2-(3-phenylpropylamino) (NPPB; 50 microM) and diphenylamine-2-carboxylic acid (DPC; 3 mM) reduced the cAMP-evoked currents by only approximately 10%. |
31(0,1,1,1) | Details |
| 8699479 | Takeuchi S, Irimajiri A: A novel, volume-correlated Cl- conductance in marginal cells dissociated from the stria vascularis of gerbils. J Membr Biol. 1996 Mar;150(1):47-62. The whole-cell Cl- current was only partially blocked by both 5-nitro-2-(3-phenylpropylamino) (NPPB, 0.5 mM) and diphenylamine-2-carboxylic acid (DPC, 1.0 mM), but 4-acetamido-4'-isothiocyanato-stilbene-2,2'-disulfonic acid (SITS, 0.5 mM) was without effect. |
31(0,1,1,1) | Details |
| 7658386 | Guinamard R, Chraibi A, Teulon J: A small-conductance Cl- channel in the mouse thick ascending limb that is activated by ATP and protein kinase A. J Physiol. 1995 May 15;485 ( Pt 1):97-112. The Cl- channel blockers 5-nitro-2-(3-phenylpropylamine)- (NPPB), 4,4'-diisothiocyanatostilbene-2,2'-disulphonic acid (DIDS) or glibenclamide, all at 0.1 mmol l-1, and diphenylamine-2-carboxylic acid (DPC), at 1 mmol l-1, inhibited the small channel activity by 80-100% in inside-out patches. 7. |
31(0,1,1,1) | Details |
| 1713412 | Singh AK, Afink GB, Venglarik CJ, Wang RP, Bridges RJ: Colonic Cl channel blockade by three classes of compounds. Am J Physiol. 1991 Jul;261(1 Pt 1):C51-63. channels were incorporated into planar lipid bilayer membranes to examine the effects of the anthranilic acids, diphenylamine 2-carboxylic acid (DPC) and 5-nitro-2-(3-phenylpropylamino) (NPPB), the indanyl alkanoic acids, 2-[(2-cyclopentyl-6,7-dichloro-2,3-dihydro-2-methyl-1-oxo-1H-inden -5-yl) oxy] (IAA-94) and its stereoenantiomer IAA-95, and the disulfonic stilbene, 4,4'-dinitro-stilbene-2,2'-disulfonic acid (DNDS). |
9(0,0,1,4) | Details |
| 11498992 | Zhou SS, Zang YM: [Effects of monocarboxylic acid derivatives on cardiac ventricular CFTR Cl- channels in guinea pig]. Sheng Li Xue Bao. 1999 Jun;51(3):297-302. Anthracene-9-carboxylic acid (9-AC) added to the bath solution further enhanced the outward component of isoproterenol-induced currents in a reversible manner, whereas 5-nitro-2-(3-phenylpropylamino) (NPPB) or diphenylamine-2-carboxylic acid (DPC) induced a biphasic effect on the currents. |
8(0,0,1,3) | Details |
| 2541404 | Gogelein H, Pfannmuller B: The nonselective cation channel in the basolateral membrane of rat exocrine pancreas. Pflugers Arch. 1989 Jan;413(3):287-98. In inside-out oriented cell-excised membrane patches the substances diphenylamine-2-carboxylic acid (DPC), 5-nitro-2-(3-phenelpropylamino)- (NPPB) and 3',5-dichlorodiphenylamine-2-carboxylic acid (DCDPC) were applied to the cytosolic side. |
7(0,0,1,2) | Details |
| 2557081 | Marcus DC, Marcus NY: Transepithelial electrical responses to Cl- of nonsensory region of gerbil utricle. Biochim Biophys Acta. 1989 Dec 11;987(1):56-62. All three agents tested, 3',5-dichlorodiphenylamine-2-carboxylic acid (DCDPC), 5-nitro-2 (3-phenylpropylamino) (NPPB) and 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS), caused an increase in Vt. |
2(0,0,0,2) | Details |
| 7562609 | Gosling M, Smith JW, Poyner DR: Characterization of a volume-sensitive current in rat osteoblast-like (ROS 17/2.8) cells. J Physiol. 1995 Jun 15;485 ( Pt 3):671-82. The volume-sensitive Cl- current was effectively inhibited by the Cl- channel blockers 4,4'- diisothiocyanatostilbene-2,2-disulphonic acid (DIDS) and 5-nitro-2-(3-phenylpropylamino) (NPPB). The current was relatively insensitive to diphenylamine-2-carboxylate (DPC), 500 microM producing only 22.5 +/- 4.0% inhibition. 5. |
2(0,0,0,2) | Details |
| 11263994 | Sasaki Y, Nagai J, Kitahara Y, Takai N, Murakami T, Takano M: Expression of chloride channel, ClC-5, and its role in receptor-mediated endocytosis of albumin in OK cells. Biochem Biophys Res Commun. 2001 Mar 23;282(1):212-8. Accumulation of fluorescein-isothiocyanate (FITC)-albumin, a receptor-mediated endocytosis marker, was inhibited by 5-nitro-2-(3-phenylpropylamino)- (NPPB), a chloride channel inhibitor, in a concentration-dependent fashion. Other chloride channel inhibitors, 4,4'-diisothiocyanatostilbene-2-2'-disulfonic acid and diphenylamine-2-carboxylic acid, also inhibited FITC-albumin uptake. |
2(0,0,0,2) | Details |
| 9618558 | Mitchell CH, Carre DA, McGlinn AM, Stone RA, Civan MM: A release mechanism for stored ATP in ocular ciliary epithelial cells. . Proc Natl Acad Sci U S A. 1998 Jun 9;95(12):7174-8. The hypotonically triggered increase in ATP was inhibited by the Cl--channel blocker 5-nitro-2-(3-phenylpropylamino) (NPPB) in both cell types. In contrast, the P-glycoprotein inhibitors tamoxifen and and the cystic fibrosis transmembrane conductance regulator (CFTR) blockers glybenclamide and diphenylamine-2-carboxylate did not affect ATP release from either cell type. |
2(0,0,0,2) | Details |
| 9888876 | Suenobu N, Shichiri M, Iwashina M, Marumo F, Hirata Y: Natriuretic peptides and induce endothelial apoptosis via a -dependent mechanism. Arterioscler Thromb Vasc Biol. 1999 Jan;19(1):140-6. Three natriuretic peptides (atrial natriuretic peptide, brain natriuretic peptide, and C-type natriuretic peptide) induced endothelial apoptosis as demonstrated by nucleosomal laddering on agarose gel electrophoresis and by the terminal deoxynucleotidyl transferase-mediated nick end labeling method. This dose-dependent relation was assessed by quantifying the fragmented and intact DNA contents by the diphenylamine method. |
1(0,0,0,1) | Details |
| 12769977 | O'Donnell MJ, Fletcher M, Haley CA: KCl reabsorption by the lower malpighian tubule of rhodnius prolixus: inhibition by Cl (-) channel blockers and acetazolamide. J Insect Physiol. 1997 Jul;43(7):657-665. The results suggest that Cl (-) reabsorption is inhibited by acetazolamide and by Cl (-) channel blockers, including diphenylamine-2-carboxylate (DPC) and 5-nitro-2-(3-phenylpropylamino) (NPPB), but not by compounds that block Na (+)/K (+)/Cl (-) and K (+)/Cl (-) co-transporters. Measurements of transepithelial potential and basolateral membrane potential during changes in bathing saline concentration indicate the presence of DPC- and NPPB-sensitive channels in the basolateral membrane. |
1(0,0,0,1) | Details |
| 8387925 | Pon DJ, Flezar M, Litster DL, Heisler S: Diphenylamine-2-carboxylate analogues block Cl- conductances in A7r5 cells by affecting cellular Ca2+ homeostasis. Eur J Pharmacol. 1993 Apr 15;245(2):119-27. The addition of a Ca2+ ionophore mimicked the -induced efflux from the cells. 5-Nitro-2-(3-phenylpropylamino)- (NPPB) and a chloro-substituted compound (cpd 149) inhibited the -stimulated 125I efflux from the cells. |
2(0,0,0,2) | Details |
| 1375638 | Sakai H, Okada Y, Morii M, Takeguchi N: and activate small-conductance Cl- channels in the basolateral membrane of rabbit parietal cells. J Physiol. 1992 Mar;448:293-306. A Cl- channel blocker, 5-nitro-2-(3-phenylpropylamino)- (NPPB) inhibited whole-cell Cl- currents. Another Cl- channel blocker, 4-acetamido-4'-isothiocyanatostilbene-2,2'-dilsulphonic acid or diphenylamine-2-carboxylate was much less effective. 4. |
2(0,0,0,2) | Details |
| 9150469 | Reeves WB: Effects of chloride channel blockers on hypoxic injury in rat proximal tubules. Kidney Int. 1997 May;51(5):1529-34. The chloride channel blocker diphenylamine-2-carboxylate (DPC) markedly reduced the degree of hypoxia-induced membrane damage as measured by the release of lactate dehydrogenase (LDH). Other Cl- channel blockers, such as niflumic acid, 5-nitro-2-(3-phenylpropylamino)- (NPPB) and 2-[(2-cyclopentyl-6,7-dichloro-2,3-dihyrdo-2-methyl-1-oxo-1H-in den-5-yl) oxy] (IAA-94) provided even greater protection than DPC and were as effective as 2 mM |
1(0,0,0,1) | Details |
| 2456807 | Wong PY: Inhibition by chloride channel blockers of anion secretion in cultured epididymal epithelium and intact epididymis of rats. Br J Pharmacol. 1988 May;94(1):155-63. Addition of diphenylamine-2-carboxylate (DPC) and 5-nitro-2-(3-phenylpropylamino)- (NPPB) caused an inhibition of the SCC when added to the apical or basolateral side. 5. |
83(1,1,1,3) | Details |
| 11504691 | Trout L, Corboz MR, Ballard ST: Mechanism of substance P-induced liquid secretion across bronchial epithelium. Am J Physiol Lung Cell Mol Physiol. 2001 Sep;281(3):L639-45. The anion channel blockers diphenylamine-2-carboxylate (DPC) and 5-nitro-2-(3-phenylpropylamino) (NPPB) inhibited > 90% of substance P-induced liquid secretion, whereas DIDS had no effect. DMA, DPC, and NPPB had greater inhibitory effects on net HCO (3)(-) secretion than on liquid secretion. |
1(0,0,0,1) | Details |
| 8661992 | Tauc M, Bidet M, Poujeol P: currents activated by calcitonin and cAMP in primary cultures of rabbit distal convoluted tubule. J Membr Biol. 1996 Apr;150(3):255-73. This current was inhibited by 10 (-3) M diphenylamine-2-carboxylate (DPC) and 10 (-4) M 5-nitro-2-(3-phenylpropylamino)- (NPPB) and was insensitive to 10 (-3) M 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS). |
82(1,1,1,2) | Details |
| 12202948 | Reddy MM, Quinton PM: Effect of anion transport blockers on CFTR in the human sweat duct. J Membr Biol. 2002 Sep 1;189(1):15-25. Studies using mostly ex vivo systems suggested diphenylamine-2-carboxylate (DPC), 5-nitro-2-(3-phenylpropylamino) (NPPB) and glybenclamide inhibit CFTR Cl- conductance (CFTR GCl). |
82(1,1,1,2) | Details |
| 10352340 | Ruckes-Nilges C, Weber U, Lindemann H, Munker G, Clauss W, Weber WM: Minor role of Cl- secretion in non-cystic fibrosis and cystic fibrosis human nasal epithelium. Cell Physiol Biochem. 1999;9(1):1-10. Under unstimulated, physiological conditions in the presence of Cl- on both sides and amiloride on the apical side of the epithelium diphenylamine-2-carboxic acid (DPC), 4,4'-diisothiocyanatostilbene-2, 2'- disulfonic acid (DIDS) and 5-nitro-2-(3-phenylpropylamino)- (NPPB) failed to induce clearcut inhibition of ISC. cAMP as well as ATP did not affect ISC either in CF or in non-CF epithelia. Reduction of apical Cl- increased ISC and depolarized transepithelial potential; however, the observed increase was insensitive to DIDS, DPC and NPPB. |
1(0,0,0,1) | Details |
| 10894792 | Rubera I, Tauc M, Bidet M, Verheecke-Mauze C, De Renzis G, Poujeol C, Cuiller B, Poujeol P: Extracellular ATP increases [Ca (2+)](i) in distal tubule cells. Am J Physiol Renal Physiol. 2000 Jul;279(1):F102-11. Diphenylamine-2-carboxylate (10 (-3) M) and NPPB (10 (-4) M) abolished the (125) I (-) efflux. |
81(1,1,1,1) | Details |
| 11487549 | Hirata K, Nathanson MH: Bile duct epithelia regulate biliary excretion in normal rat liver. Gastroenterology. 2001 Aug;121(2):396-406. The effects of were blocked by 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid (DIDS), 5-nitro2-(3-phenylpropylamino) (NPPB), or diphenylamine-2-carboxylic acid (DPC), and the effects of secretin were inhibited by NPPB or DPC and unaffected by DIDS. |
81(1,1,1,1) | Details |
| 7864157 | Wang T, Segal AS, Giebisch G, Aronson PS: Stimulation of transport by cAMP in rat proximal tubules. Am J Physiol. 1995 Feb;268(2 Pt 2):F204-10. In contrast, the increments in Jv and JCl due to dibutyryl cAMP were abolished by luminal 5-nitro-2-(3-phenylpropylamino) (NPPB; 10 microM), another Cl- channel blocker. We have previously demonstrated that and stimulate transcellular Cl- absorption (JCl) in the rat proximal tubule by a mechanism involving DIDS-sensitive anion exchange across the luminal membrane and diphenylamine-2-carboxylate (DPC)-sensitive Cl- channels in the basolateral membrane. |
1(0,0,0,1) | Details |
| 2481731 | Giraldez F, Murray KJ, Sepulveda FV, Sheppard DN: Characterization of a phosphorylation-activated Cl-selective channel in isolated Necturus enterocytes. J Physiol. 1989 Sep;416:517-37. channels in excised inside-out patches were inhibited by stilbene and diphenylamine-2-carboxylate derivatives. 4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulphonic acid (SITS, 5 x 10 (-5) M) and 5-nitro-2-(3-phenylpropylamino) (NPPB, 1 x 10 (-5) M) caused an irreversible 'flickery' blockade without altering single-channel current. 3'5-Dichlorodiphenylamine-2-carboxylic acid (DDPC, 5 x 10 (-5) M) reduced the currents at every voltage without apparent effects on gating properties of the channel.(ABSTRACT TRUNCATED AT 400 WORDS) |
81(1,1,1,1) | Details |
| 10644658 | Meng X, Reeves WB: Effects of chloride channel inhibitors on H (2) O (2)-induced renal epithelial cell injury. Am J Physiol Renal Physiol. 2000 Jan;278(1):F83-90. Substitution of Cl (-) by or the inclusion of certain Cl (-) channel blockers, e.g., diphenylamine-2-carboxylate (DPC), 5-nitro-2-(3-phenylpropylamino). (NPPB), and niflumic acid, prevented the H (2) O (2)-induced loss of membrane integrity to LDH. |
81(1,1,1,1) | Details |
| 9277352 | Kokko KE, Matsumoto PS, Zhang ZR, Ling BN, Eaton DC: increases 7-pS Cl- channel density in the apical membrane of A6 distal nephron cells. Am J Physiol. 1997 Aug;273(2 Pt 1):C548-57. The effect was only partially abolished by either apical amiloride, an Na+ channel blocker, or 5-nitro-2-(3-phenylpropylamino) (NPPB), a Cl- channel blocker. The channel was blocked by diphenylamine-2-carboxylate, glibenclamide, and NPPB but not by 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid. |
1(0,0,0,1) | Details |
| 8313229 | Wang X, Fedorko L, Marunaka Y, O'Brodovich H: Whole-cell Cl- currents in a human peripheral airway epithelial cell line. Can J Physiol Pharmacol. 1993 Sep;71(9):662-70. Diphenylamine-2-carboxylate (10 (-4) M) applied intracellularly blocked the outward-rectified current, while extracellularly applied diphenylamine-2-carboxylate had no effect on Cl- current. This current was also blocked by extracellularly applied 5-nitro-2-(3-phenylpropylamino) (NPPB), with an estimated IC50 of 15.2 microM. |
1(0,0,0,1) | Details |