Name | AP 1 (protein family or complex) |
---|---|
Synonyms | AP 1; AP 1 complex; AP1; Adapter related protein complex 1 |
Name | 4-aminopyridine |
---|---|
CAS | 4-pyridinamine |
PubMed | Abstract | RScore(About this table) | |
---|---|---|---|
12802579 | Kwan CY, Zhang WB, Kwan TK, Sakai Y: In vitro relaxation of vascular smooth muscle by atropine: involvement of K+ channels and endothelium. Naunyn Schmiedebergs Arch Pharmacol. 2003 Jul;368(1):1-9. Epub 2003 Jun 11. Pretreatment of +E aorta with tetraethylammonia (TEA, 3-10 mM) or 4-aminopyridine (4-AP, 1-3 mM) showed prominent inhibitory effect on atropine-induced relaxation; on the other hand, preincubation with glibenclamide (1-10 microM), BaCl (2) (1-30 microM) or 2 microM charybdotoxin and apamin, had little effect on the relaxation induced by atropine. |
31(0,1,1,1) | Details |
10835337 | Cornfield DN, Saqueton CB, Porter VA, Herron J, Resnik E, Haddad IY, Reeve HL: Voltage-gated K (+)-channel activity in ovine pulmonary vasculature is developmentally regulated. Am J Physiol Lung Cell Mol Physiol. 2000 Jun;278(6):L1297-304. To determine developmental changes in K (v)-channel activity, the effects of the K (+)-channel antagonist 4-aminopyridine (4-AP) were studied on fetal and adult PASMC [Ca (2+)](i). 4-AP (1 mM) caused PASMC [Ca (2+)](i) to increase by 94 +/- 22% in the fetus and 303 +/- 46% in the adult. |
31(0,1,1,1) | Details |
12466248 | Wang SJ, Coutinho V, Sihra TS: Presynaptic cross-talk of beta-adrenoreceptor and 5-hydroxytryptamine receptor signalling in the modulation of release from cerebrocortical nerve terminals. Br J Pharmacol. 2002 Dec;137(8):1371-9. The presynaptic interactions between facilitatory beta-adrenoreceptors and inhibitory receptors modulating release from cerebrocortical nerve terminals were examined. 2. 4-aminopyridine (4-AP, 1 mM)-evoked release was facilitated by the membrane permeant cyclic-3',5'- (cAMP) analogue, 8-bromo-cAMP (8-Br-cAMP), used to directly activate cAMP-dependent protein kinase (PKA). 3. |
31(0,1,1,1) | Details |
18832757 | Heaps CL, Jeffery EC, Laine GA, Price EM, Bowles DK: Effects of exercise training and hypercholesterolemia on activation of voltage-dependent K+ channels in coronary arterioles. J Appl Physiol. 2008 Dec;105(6):1761-71. Epub 2008 Oct 2. Arterioles ( approximately 150 mum) from both HC-Sed and HC-Ex pigs displayed impaired -mediated dilatation that was attributable to the elimination of 4-aminopyridine (4-AP; 1 mM)-sensitive Kv channel activation compared with NC counterparts. |
0(0,0,0,0) | Details |
10900178 | Workman AJ, Kane KA, Rankin AC: Rate-dependency of action potential duration and refractoriness in isolated myocytes from the rabbit AV node and atrium. J Mol Cell Cardiol. 2000 Aug;32(8):1525-37. The aims of this study were to investigate the rate-dependency of the action potential duration (APD) and effective refractory period (ERP) in single myocytes isolated from the AV node and atrium of rabbit hearts, using whole cell patch clamping, and to determine the contribution of the 4-aminopyridine (4-AP)-sensitive current, I (TO1) to these relationships in the two cell types. |
0(0,0,0,0) | Details |
12967944 | Hashitani H, Brading AF: Electrical properties of detrusor smooth muscles from the pig and human urinary bladder. Br J Pharmacol. 2003 Sep;140(1):146-58. Epub 2003 Jun 9. Charybdotoxin (CTX, 50 nm) increased the amplitude and duration of action potentials but failed to inhibit the fast AHPs, while apamin (0.1 microm) blocked the fast AHPs and induced action potential complexes, which were followed by slow AHPs. 4-Aminopyridine (4-AP, 1 mm) suppressed the slow AHP and increased action potential frequency. (4) In the human bladder, transmural stimuli initiated inhibitory junction potential-like hyperpolarizations, which were followed by action potential discharges. |
0(0,0,0,0) | Details |
18577383 | Gupta PK, Subramani J, Leo MD, Sikarwar AS, Parida S, Prakash VR, Mishra SK: Role of voltage-dependent gap junctions in 4-aminopyridine-induced inhibition of relaxation in rat carotid artery. Eur J Pharmacol. 2008 Sep 4;591(1-3):171-6. Epub 2008 Jun 12. |
channels and myo-endothelial 0(0,0,0,0) | Details |
12185007 | St -John WM, Rybak IA, Paton JF: Potential switch from eupnea to fictive gasping after blockade of transmission and channels. Am J Physiol Regul Integr Comp Physiol. 2002 Sep;283(3):R721-31. To block channels, 4-aminopyridine (4-AP, 1-10 microM) was administered. |
31(0,1,1,1) | Details |
10952691 | Dong H, Jiang Y, Cole WC, Triggle CR: Comparison of the pharmacological properties of EDHF-mediated vasorelaxation in guinea-pig cerebral and mesenteric resistance vessels. Br J Pharmacol. 2000 Aug;130(8):1983-91. In cerebral arteries, charybdotoxin (ChTX; 0.1 microM) completely inhibited the indomethacin, L-NNA and ODQ-insensitive relaxation; iberiotoxin (IbTX, 0.1 microM), 4-aminopyridine (4-AP, 1 mM), or barium (30 microM) significantly reduced the response; in the mesenteric artery, ChTX and IbTX also reduced this relaxation. |
31(0,1,1,1) | Details |
19377272 | Adaramoye OA, Medeiros IA: Endothelium-independent vasodilation induced by kolaviron, a biflavonoid complex from Garcinia kola seeds, in rat superior mesenteric arteries. J Smooth Muscle Res. 2009 Feb;45(1):39-53. Also, the vasorelaxation induced by KV was significantly inhibited after pre-treatment of the denuded rings with 4-aminopyridine (4-AP) 1 mM, a selective blocker of voltage-dependent K (+) (K (v)) channels and, tetraethylammonium (TEA) 1 mM or charybdotoxin (ChTX) 0.1 microM, non-selective blockers of large and intermediate conductance Ca (2+)-activated K (+) (BK (Ca)) channels. |
31(0,1,1,1) | Details |
12595962 | Horinouchi T, Tanaka Y, Koike K: Evidence for the primary role for 4-aminopyridine-sensitive K (v) channels in beta (3)-adrenoceptor-mediated, cyclic AMP-independent relaxations of guinea-pig gastrointestinal smooth muscles. Naunyn Schmiedebergs Arch Pharmacol. 2003 Feb;367(2):193-203. Epub 2003 Jan 14. On the other hand, the SQ-22536-resistant, beta (3)-adrenoceptor-mediated relaxant components were potently attenuated when the tone was raised using high-KCl (80 mM) or in the presence of a K (v) channel blocker, 4-aminopyridine (4-AP, 1-3 mM). |
31(0,1,1,1) | Details |
11411493 | Yeon D, Kwon S, Lee Y, Leem J, Nam T, Ahn D: coronary artery. . J Vet Med Sci. 2001 May;63(5):499-503. However, application of 4-aminopyridine (4-AP, 1 mM), a blocker of delayed rectifier K+ current significantly inhibited the -induced relaxation with concomitant attenuation of the effect on intracellular Ca2+ concentration. |
-induced relaxation in rabbit 31(0,1,1,1) | Details |
17533425 | Nguyen DT, Lang RJ, Exintaris B: K+ channel modulation of slow wave activity in the guinea-pig prostate. . Br J Pharmacol. 2007 Jul;151(6):828-36. Epub 2007 May 29. KEY RESULTS: Tetraethylammonium (TEA 300 micro M and 1 mM), iberiotoxin (150 nM) and 4-aminopyridine (4-AP 1 mM) increased the frequency of slow wave discharge. |
7(0,0,1,2) | Details |
10720882 | Shimizu S, Yokoshiki H, Sperelakis N, Paul RJ: Role of voltage-dependent and Ca (2+)-activated K (+) channels on the regulation of isometric force in porcine coronary artery. J Vasc Res. 2000 Jan-Feb;37(1):16-25. Isometric force and intracellular Ca (2+) ([Ca (2+)](i)) under resting conditions were increased by treatment with 4-aminopyridine (4-AP, 1 mM), an inhibitor of voltage-dependent K (+) (K (v)) channels, but not by tetraethylammonium (TEA, 1 mM) or charybdotoxin (100 nM), both inhibitors of Ca (2+)-activated K (+) (K (Ca)) channels, or glibenclamide (10 microM), an inhibitor of ATP-sensitive K (+) channels. |
0(0,0,0,0) | Details |
19252101 | Favaloro JL, Kemp-Harper BK: Redox variants of NO (NO{middle dot} and HNO) elicit vasorelaxation of resistance arteries via distinct mechanisms. Am J Physiol Heart Circ Physiol. 2009 May;296(5):H1274-80. Epub 2009 Feb 27. Both vasorelaxation and repolarization responses to Angeli's salt were significantly attenuated by both the HNO scavenger (3 mM) and the voltage-dependent K (+) (K (v)) channel inhibitor 4-aminopyridine (4-AP; 1 mM) and virtually abolished by the soluble guanylate cyclase (sGC) inhibitor 1H-[1,2,4] oxadiazolo [4,3-a] quinoxalin-1-one (ODQ; 10 microM) or 30 mM K (+). |
0(0,0,0,0) | Details |
11744003 | Moe MC, Berg-Johnsen J, Roste GK, Vinje ML: Stimulated increase in free cytosolic Ca (2+) and protein kinase C activity in human cerebrocortical synaptosomes. Brain Res. 2002 Jan 4;924(1):116-9. Membrane depolarisation by 4-aminopyridine (4-AP) 1 mM increased the [Ca (2+)](i) fluorescence by 14.4+/-2.2% and the PKC activity fluorescence by 16.7+/-1.6%. |
7(0,0,1,2) | Details |
15085060 | Franke R, Yang Y, Rubin LJ, Magliola L, Jones AW: High-fat diet alters K+-currents in porcine coronary arteries and inhibition. J Cardiovasc Pharmacol. 2004 Apr;43(4):495-503. To determine the involvement of K+-channels, ADO responses were measured in the presence of 4-aminopyridine (4-AP, 1 mM) or glybenclamide (GLYB, 10 microM). |
sensitivity during metabolic 6(0,0,1,1) | Details |
16697949 | Yildiz O, Nacitarhan C, Seyrek M: levosimendan on the human umbilical artery. J Soc Gynecol Investig. 2006 May;13(4):312-5. Levosimendan-induced relaxations were tested in the presence of the large conductance Ca2+-activated K+ channel inhibitor tetraethylammonium (TEA, 1 mM), the (ATP)-sensitive K+ channel inhibitor glibenclamide (GLI, 10 microM), and the voltage-sensitive K+ channel inhibitor 4-aminopyridine (4-AP, 1 mM). |
channels in the vasodilating action of 32(0,1,1,2) | Details |
15897786 | Yildiz O, Seyrek M, Gul H, Un I, Yildirim V, Ozal E, Uzun M, Bolu E: artery in vitro. J Cardiovasc Pharmacol. 2005 Jun;45(6):580-5. -induced relaxations were tested in the presence of cyclooxygenase inhibitor indomethacin (10 microM), synthase inhibitor Nomega-nitro- methyl ester (L-NAME, 1 microM), nonselective large-conductance Ca2+-activated and voltage-sensitive K+ channel inhibitor tetraethylammonium (TEA, 1 mM), ATP-sensitive K+ channel inhibitor glibenclamide (GLI, 100 microM), and voltage-sensitive K+ channel inhibitor 4-aminopyridine (4-AP, 1 mM). |
relaxes human internal mammary 31(0,1,1,1) | Details |
17380036 | Seyrek M, Yildiz O, Ulusoy HB, Yildirim V: artery by potassium channel opening action. J Pharmacol Sci. 2007 Mar;103(3):309-16. -induced relaxations were tested in the presence of the cyclooxygenase inhibitor indomethacin (10 microM), synthase inhibitor N (omega)-nitro- methyl ester (L-NAME, 100 microM), non-selective large conductance Ca (2+)-activated and voltage-sensitive K (+) channel inhibitor tetraethylammonium (TEA, 1 mM), ATP-sensitive K (+) channel inhibitor glibenclamide (GLI, 10 microM), and voltage-sensitive K (+) channel inhibitor 4-aminopyridine (4-AP, 1 mM). |
relaxes isolated human radial 31(0,1,1,1) | Details |
17602893 | Lunardi CN, Vercesi JA, da Silva RS, Bendhack LM: Vasorelaxation induced by the new activation of K (Ca) by a -dependent pathway. Vascul Pharmacol. 2007 Aug-Sep;47(2-3):139-44. Epub 2007 Jun 2. Relaxation stimulated with RUNOCL was also studied on 60 mM of KCl-contracted arteries or after incubation with the non-selective K (+) channel blocker (1 mM TEA) or the selective K (+) channel blockers (3 microM glibenclamide (K (ATP)), 1 mM 4-aminopyridine (K (V), 4-AP), 1 microM apamin (SK (Ca)-APA) or 0.1 microM iberiotoxin (BK (Ca) IBTX). |
donor cis-[Ru (Cl)(bpy)(2)(NO)](PF (6)) is due to 6(0,0,1,1) | Details |
17893456 | Spohr F, Busch CJ, Reich C, Motsch J, Gebhard MM, Kuebler WM, Bloch KD, Weimann J: 4-Aminopyridine restores impaired hypoxic pulmonary vasoconstriction in endotoxemic mice. Anesthesiology. 2007 Oct;107(4):597-604. Analysis of pulmonary vascular pressure-flow curves revealed that 4-AP (1) counteracted the observed lipopolysaccharide-induced changes in alpha and R0 under normoxic conditions and (2) augmented the hypoxia-induced increase in R0 in lungs of endotoxemic mice. |
1(0,0,0,1) | Details |
17638013 | Biella GR, Spaiardi P, Jimenez-Moreno R, Magistretti J, Taglietti V, Toselli M: A fast transient outward current in layer II/III neurons of rat perirhinal cortex. Pflugers Arch. 2007 Dec;455(3):515-25. Epub 2007 Jul 19. Application of 4-AP (1-5 mM) reversibly and selectively blocked I (A), and in current clamp conditions it increased spike duration and shortened the delay of the first spike during repetitive firing evoked by sustained depolarizing current injection. |
1(0,0,0,1) | Details |
12072589 | Bardou M, Goirand F, Bernard A, Guerard P, Gatinet M, Devillier P, Dumas JP, Morcillo EJ, Rochette L, Dumas M: Relaxant effects of selective phosphodiesterase inhibitors on U46619 precontracted human intralobar pulmonary arteries and role of channels. J Cardiovasc Pharmacol. 2002 Jul;40(1):153-61. All PDEI tested induced a concentration-dependent relaxation with being significantly (p < 0.05) more efficient and rolipram more potent than PDE5I and PDE3I (Emax values, expressed as a percentage of maximal relaxation by papaverine 10 (-4) M, were 92% +/- 2%, 84% +/- 8%, 90% +/- 4% and 99% +/- 1%, and pD2 values were 7.30 +/- 0.35, 6.14 +/- 0.25, 5.86 +/- 0.17, and 4.85 +/- 0.47 for rolipram, siguazodan, zaprinast and respectively). 4-Aminopyridine (4-AP, Kv, voltage dependent channel blocker, 1 mM) induced a significant increase (+17% p < 0.05) of U46619-induced vasoconstriction whereas the other K+-channels blockers, glibenclamide (KATP channels, 1 microM) charybdotoxin (predominant BKCa, large conductance Ca2+-sensitive K+ channels, 0.1 microM) and apamine (SKCa, small conductance, 0.3 microM) were without effect. The concentration response curves (CRC) for rolipram were significantly shifted to the right by glibenclamide (1 microM), charybdotoxin (0.1 microM) and 4-AP (1 mM). |
1(0,0,0,1) | Details |
11744755 | Daniel H, Crepel F: Control of Ca (2+) influx by cannabinoid and metabotropic glutamate receptors in rat cerebellar cortex requires K (+) channels. J Physiol. 2001 Dec 15;537(Pt 3):793-800. Bath application of the potassium channel blocker 4-AP (1 mM) totally prevented both the WIN55,212-2- and the L-AP4-induced inhibition of peak fluorescence transients evoked by parallel fibre stimulation. 5. |
1(0,0,0,1) | Details |
10960595 | Sanz AG, Hospital S, Badia A, Clos MV: Presynaptic effect of 7-OH-DPAT on evoked [3H]- The objective of the present experiments was to study the presynaptic effect of 7- -N,N-di-n-propyl-2-aminotetraline (7-OH-DPAT, a D (2)-like receptor agonist) on [3H]- ([3H]- release induced by (15 mM, 25 mM and 60 mM), potassium channel-blockers (4-aminopyridine, 4-AP; tetraethylammonium, TEA and quinine) and veratridine to gain insight into the mechanisms involved in the activation of the D (2) -receptor subtype located at striatal cholinergic nerve terminals. 7-OH-DPAT (1 microM) inhibited the evoked [3H]- release induced by K (+) 15 mM in a similar percentage than that obtained during basal conditions (30% and 27%, respectively). Nevertheless, in the presence of 25 mM and 60 mM of K (+) the inhibitory effect of 7-OH-DPAT was completely abolished. 4-AP (1-100 microM) and TEA (1 and 5 mM) significantly enhanced [3H]- release, showing 69.32%+/-7.60% (P <0.001) and 52.27%+/-5.64% (P <0.001), respectively, at the highest concentrations tested. |
release in rat striatal synaptosomes. Brain Res. 2000 Aug 25;874(2):116-22.1(0,0,0,1) | Details |
17258511 | Pimentel AM, Costa CA, Carvalho LC, Brandao RM, Rangel BM, Tano T, Soares de Moura R, Resende AC: The role of NO-cGMP pathway and clonidine in the rat mesenteric arterial bed. Vascul Pharmacol. 2007 May;46(5):353-9. Epub 2006 Dec 20. In contrast, the vasodilation induced by clonidine was not affected by voltage-dependent K+ channels (K (V)) blocker, 4-aminopyridine (4-AP, 1 mM). |
channels on the relaxation induced by 0(0,0,0,0) | Details |
11834621 | Tep-areenan P, Kendall DA, Randall MD: mediated predominantly via channels. Br J Pharmacol. 2002 Feb;135(3):735-40. A selective inhibitor of ATP-sensitive K (+) (K (ATP)) channels, glibenclamide (10 microM) and an inhibitor of voltage-sensitive K (+) (K (V)) channels, 4-aminopyridine (4-AP, 1 mM) did not affect -induced responses. |
-induced vasorelaxation in the rat mesenteric arterial bed is 0(0,0,0,0) | Details |