| Name | cytochrome P450 (protein family or complex) |
|---|---|
| Synonyms | cytochrome P450; cytochrome P 450; CYP450; CYP 450 |
| Name | 4-aminopyridine |
|---|---|
| CAS | 4-pyridinamine |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 16042987 | Gendron G, Gobeil F Jr, Belanger S, Gagnon S, Regoli D, D'Orleans-Juste P: Urotensin II-induced hypotensive responses in Wistar-Kyoto (Wky) and spontaneously hypertensive (Shr) rats. Peptides. 2005 Aug;26(8):1468-74. These include the non-selective synthase inhibitor L-NAME (5 micromol/kg), the non-selective cyclooxygenase inhibitor meclofenamate (16 micromol/kg), the voltage-sensitive and ATP-sensitive K+-channel inhibitors, 4-aminopyridine (5 micromol/kg) and glybenclamide (10 micromol/kg), the cytochrome P450 CYP2C9 inhibitor sulfaphenazole (15 micromol/kg), the cytoskeletal fixation agent phalloidin (15 micromol/kg), the endothelin ETB receptor antagonist BQ-788 (35 micromol/kg), the bradykinin B2 receptor antagonist HOE 140 (0.5 micromol/kg), the angiotensin AT2 antagonist PD 123319 (10 micromol/kg) and the UT receptor antagonist urantide (10 micromol/kg). |
31(0,1,1,1) | Details |
| 12913062 | Souza HC, Salgado HC, Ballejo G, Salgado MC: SR141716A-sensitive enhancement of ET-1 hypotensive effect by chronic NOS inhibition. Hypertension. 2003 Oct;42(4):802-5. Epub 2003 Aug 11. The enhanced ET-1 hypotensive effect in L-NAME-treated rats was abolished by the ETB receptor antagonist BQ-788 but was unaltered by the cyclooxygenase inhibitor diclofenac, the cytochrome P450 inhibitor fluconazole, or the potassium channel blockers apamin, glibenclamide, tetraethylammonium, and 4-aminopyridine. |
31(0,1,1,1) | Details |
| 12629172 | Gebremedhin D, Yamaura K, Zhang C, Bylund J, Koehler RC, Harder DR: Metabotropic glutamate receptor activation enhances the activities of two types of Ca2+-activated k+ channels in rat hippocampal astrocytes. J Neurosci. 2003 Mar 1;23(5):1678-87. Patch-clamp analysis of K (+) channel currents in cultured astrocytes identified the existence of 71 +/- 6 and 161 +/- 11 pS single-channel K (+) currents that were sensitive to changes in voltage and [Ca (2+)](i) and blocked by external TEA but not by charybdotoxin, iberiotoxin, apamin, or 4-aminopyridine. Activation of the two types of K (+) channel currents by mGluR agonists was attenuated by pertussis toxin and by inhibition of phospholipase C (PLC) or cytochrome P450 epoxygenase. |
2(0,0,0,2) | Details |
| 11668080 | Chlopicki S, Nilsson H, Mulvany MJ: Initial and sustained phases of myogenic response of rat mesenteric small arteries. Am J Physiol Heart Circ Physiol. 2001 Nov;281(5):H2176-83. A possible role for a metabolite of cytochrome P-450 omega-hydroxylase in the initial and sustained phases of the myogenic response in cannulated rat mesenteric small arteries was studied. Apamin, glibenclamide, 4-aminopyridine, and barium had no effect on either phase. |
2(0,0,0,2) | Details |
| 17035095 | Moroe H, Honda H: Comparison of endothelial function in the carotid artery between normal and short-term hypercholesterolemic rabbits. Comp Biochem Physiol C Toxicol Pharmacol. 2006 Oct;144(2):197-203. Epub 2006 Sep 3. The resistant part of -induced relaxation was significantly inhibited when the carotid artery was treated with glibenclamide, a selective inhibitor of ATP-sensitive K (+) channels, 4-aminopyridine, an inhibitor of voltage-dependent K (+) channels, or charybdotoxin, an inhibitor of large and intermediate conductance Ca (2+)-activated K (+) channels, and it was significantly inhibited by tetraethylammonium, a non-selective inhibitor of Ca (2+)-activated K (+) channels and N,N-di-ethylaminoethyl-2,2-diphenylvalerate hydrochloride (SKF 525a), a nonselective cytochrome P-450 monooxygenase (CYP) inhibitor, or ketoconazole, a selective CYP3A inhibitor in only normal rabbits. The resistant part of -induced relaxation was significantly inhibited when the carotid artery was treated with glibenclamide, a selective inhibitor of ATP-sensitive K (+) channels, 4-aminopyridine, an inhibitor of voltage-dependent K (+) channels, or charybdotoxin, an inhibitor of large and intermediate conductance Ca (2+)-activated K (+) channels, and it was significantly inhibited by tetraethylammonium, a non-selective inhibitor of Ca (2+)-activated K (+) channels and N,N-di-ethylaminoethyl-2,2-diphenylvalerate hydrochloride (SKF 525a), a nonselective cytochrome P-450 monooxygenase (CYP) inhibitor, or ketoconazole, a selective CYP3A inhibitor in only normal rabbits. |
1(0,0,0,1) | Details |
| 11882617 | Lauterbach B, Barbosa-Sicard E, Wang MH, Honeck H, Kargel E, Theuer J, Schwartzman ML, Haller H, Luft FC, Gollasch M, Schunck WH: Cytochrome P450-dependent metabolites are novel BK channel activators. Hypertension. 2002 Feb;39(2 Pt 2):609-13. The effect of 17 (R),18 (S)-EETeTr was blocked by tetraethylammonium but not by 4-aminopyridine. |
1(0,0,0,1) | Details |
| 10611413 | Fujimoto S, Ikegami Y, Isaka M, Kato T, Nishimura K, Itoh T: K (+) channel blockers and cytochrome P450 inhibitors on -induced, endothelium-dependent relaxation in rabbit mesenteric artery. Eur J Pharmacol. 1999 Nov 12;384(1):7-15. The -induced relaxation was also inhibited with tetraethylammonium, 4-aminopyridine and charybdotoxin, but not with Ba (2+), apamin, iberiotoxin nor glibenclamide. |
1(0,0,0,1) | Details |
| 16497109 | Gerova M, Kittova M: Systemic blood pressure response to the inhibition of two hyperpolarizing pathways: a comparison to NO-synthase inhibition. Physiol Res. 2006;55(6):603-10. After the inhibition of the action voltage-dependent K (+) channels operator by 4-aminopyridine 0.1 mg/100 g b.w. , the other hyperpolarizing pathway, blood pressure declined slightly from 132.3+/-3.2 mm Hg to 116.5+/-5.0 mm Hg, P <0.05 . |
0(0,0,0,0) | Details |
| 11568792 | Fulep EE, Vedernikov YP, Saade GR, Garfield RE: The role of endothelium-derived hyperpolarizing factor in the regulation of the uterine circulation in pregnant rats. Am J Obstet Gynecol. 2001 Sep;185(3):638-42. RESULTS: The decrease in perfusion pressure induced by endothelium-derived hyperpolarizing factor was significantly attenuated by 4-aminopyridine and was abolished by a combination of 4-aminopyridine and tetraethylammonium. |
0(0,0,0,0) | Details |
| 15464071 | Guerard P, Goirand F, Fichet N, Bernard A, Rochette L, Morcillo EJ, Dumas M, Bardou M: relaxes human pulmonary arteries through K+ channels and pathways. Eur J Pharmacol. 2004 Oct 6;501(1-3):127-35. -induced relaxation was significantly inhibited by glibenclamide (1 microM, ATP-dependent K (+) channel (K (ATP)) blocker), apamin and charybdotoxin (0.3 microM small (SK (Ca)) and 0.1 microM big (BK (Ca)) conductance Ca (2+)-sensitive K (+) channel blocker, respectively), and 4-aminopyridine (1 mM, voltage-dependent K (+) channel (K (V)) blocker). |
0(0,0,0,0) | Details |
| 10903955 | Jiang F, Li CG, Rand MJ: Mechanisms of -independent relaxations induced by carbachol and in rat isolated renal arteries. Br J Pharmacol. 2000 Jul;130(6):1191-200. These relaxations were not altered by 4-aminopyridine (4-AP), glibenclamide or apamin. |
0(0,0,0,0) | Details |