| Name | sodium channel (protein family or complex) |
|---|---|
| Synonyms | Sodium channel |
| Name | diphenylamine |
|---|---|
| CAS |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 17035036 | Hudgens DP, Taylor C, Batts TW, Patel MK, Brown ML: Discovery of diphenyl amine based sodium channel blockers, effective against hNav1.2. Bioorg Med Chem. 2006 Dec 15;14(24):8366-78. Epub 2006 Oct 10. |
3(0,0,0,3) | Details |
| 9706740 | Reddix RA, Mullet D, Fertel R, Cooke HJ: Endogenous inhibits endothelin-1-induced secretion in guinea pig colon. Nitric Oxide. 1998;2(1):28-36. The reduction in Isc in response to hemoglobin was reversed by and blockers of secretion, including bumetanide and diphenylamine-2-carboxylic acid, but not by the potassium channel blockers, barium and tetraethylammonium, nor by amiloride, an epithelial sodium channel blocker. |
0(0,0,0,0) | Details |
| 14695481 | Xing Y, He Q, Zhu JX, Chan HC: Basolateral membrane mechanisms involved in ligustrazine-stimulated anion secretion in rat distal colon. Sheng Li Xue Bao. 2003 Dec 25;55(6):653-7. In freshly isolated colonic strips, basolateral addition of ligustrazine stimulated a rise in I (SC), which was resistant to basolateral application of neuronal sodium channel blocker tetrodotoxin (TTX), but inhibited by 55.2% by basolateral pretreatment with prostaglandin inhibitor indomethacin. The ligustrazine-induced I (SC) increase was inhibited by apical application of Cl (-) channel blockers diphenylamine-2,2'-dicarboxylic acid (DPC) and glibenclamide. |
1(0,0,0,1) | Details |
| 12466941 | Cuffe JE, Howard DP, Bertog M, Korbmacher C: Basolateral adrenoceptor activation mediates -induced Cl- secretion in M-1 mouse cortical collecting duct cells. Pflugers Arch. 2002 Dec;445(3):381-9. Epub 2002 Nov 1. Steady-state I (SC) averaged 87.5+/-2.9 microA cm (-2) (n=185) and was reduced by 97.1+/-0.1% (n=80) by apical amiloride (100 microM) confirming that the predominant electrogenic transport across M-1 monolayers is absorption via the epithelial sodium channel (ENaC). In contrast, the response was largely reduced in the presence of apical diphenylamine-2-carboxylic acid (1 mM) and in the absence of extracellular Cl (-). |
1(0,0,0,1) | Details |
| 12183480 | Phillips JE, Hey JA, Corboz MR: Effects of ion transport inhibitors on MCh-mediated secretion from porcine airway submucosal glands. J Appl Physiol. 2002 Sep;93(3):873-81. When the epithelium was pretreated for 3 min with the sodium channel blocker amiloride, the methacholine (1,000 microM)-induced J (G) increased to 0.67 +/- 0.09 microl. min (-1). cm (-2), and the hyperpolarization increased to 2.2 +/- 0.5 mV over the amiloride-pretreated level. When pretreated for 3 min with the chloride channel blocker diphenylamine-2-carboxylic acid, the methacholine (1,000 microM)-induced J (G) was inhibited to 0.20 +/- 0.06 microl. min (-1). cm (-2), and the methacholine-induced hyperpolarization was abolished. |
1(0,0,0,1) | Details |