| Name | phosphodiesterase |
|---|---|
| Synonyms | CAMP specific phosphodiesterase variant PDE4A 10; CAMP specific phosphodiesterase variant TM3; CAMP specific phosphodiesterase; Cyclic AMP phosphodiesterase PDE4A11; Cyclic AMP specific phosphodiesterase HSPDE4A10; DPDE 2; DPDE2; PDE 4… |
| Name | 4-aminopyridine |
|---|---|
| CAS | 4-pyridinamine |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 11790809 | Lien CC, Martina M, Schultz JH, Ehmke H, Jonas P: Gating, modulation and subunit composition of voltage-gated K (+) channels in dendritic inhibitory interneurones of rat hippocampus. J Physiol. 2002 Jan 15;538(Pt 2):405-19. Voltage-gated K (+) currents in nucleated patches isolated from OA interneurones consisted of three major components: a fast delayed rectifier K (+) current component that was highly sensitive to external 4-aminopyridine (4-AP) and tetraethylammonium (TEA) (half-maximal inhibitory concentrations < 0.1 mM for both blockers), a slow delayed rectifier K (+) current component that was sensitive to high concentrations of TEA, but insensitive to 4-AP, and a rapidly inactivating A-type K (+) current component that was blocked by high concentrations of 4-AP, but resistant to TEA. Coapplication of the membrane-permeant cAMP analogue 8-(4-chlorophenylthio)- 3':5'-cyclic monophosphate (cpt-cAMP) and the phosphodiesterase blocker isobutyl-methylxanthine (IBMX) resulted in a selective inhibition of the fast delayed rectifier K (+) current component. |
1(0,0,0,1) | Details |
| 11770009 | Yamaki F, Kaga M, Horinouchi T, Tanaka H, Koike K, Shigenobu K, Toro L, Tanaka Y: MaxiK channel-mediated relaxation of guinea-pig aorta following stimulation of IP receptor with beraprost via cyclic AMP-dependent and -independent mechanisms. Naunyn Schmiedebergs Arch Pharmacol. 2001 Dec;364(6):538-50. The relaxation induced by beraprost was not significantly affected by other K+ channel blockers glibenclamide (10 (-6) M) or Ba2+ (10 (-5) M), but was slightly attenuated by 4-aminopyridine (10 (-4) M). A selective inhibitor of cyclic AMP-specific phosphodiesterase, RO-20-1724 (10 (-4) M), significantly potentiated beraprost-induced relaxation. |
1(0,0,0,1) | Details |
| 11770006 | Costa G, Labadia A, Triguero D, Jimenez E, Garcia-Pascual A: Nitrergic relaxation in urethral smooth muscle: involvement of channels and alternative redox forms of NO. Naunyn Schmiedebergs Arch Pharmacol. 2001 Dec;364(6):516-23. Relaxation evoked by EFS of nitrergic nerves or by exogenous NO was not inhibited by any of the K+ channel blockers, but was enhanced by 4-aminopyridine [inhibitor of voltage-dependent K+ (KV) channels]. |
0(0,0,0,0) | Details |
| 11219402 | Blandizzi C, Colucci R, Tognetti M, De Paolis B, Del Tacca M: H3 receptor-mediated inhibition of intestinal release: pharmacological characterization of signal transduction pathways. Naunyn Schmiedebergs Arch Pharmacol. 2001 Feb;363(2):193-202. Tetraethylammonium or 4-aminopyridine, acting as inhibitors of voltage-dependent K+ channels, enhanced the evoked tritium outflow when tested alone, and apparently counteracted the inhibitory effect of |
0(0,0,0,0) | Details |
| 16247764 | Wang SJ: An investigation into the effect of the type IV phosphodiesterase inhibitor rolipram in the modulation of release from rat prefrontocortical nerve terminals. Synapse. 2006 Jan;59(1):41-50. In prefrontocortical nerve terminals, rolipram potentiated the Ca (2+)-dependent release of evoked by 4-aminopyridine (4AP) in a concentration-dependent manner. |
3(0,0,0,3) | Details |
| 11483882 | Bardou M, Goirand F, Marchand S, Rouget C, Devillier P, Dumas JP, Morcillo EJ, Rochette L, Dumas M: Hypoxic vasoconstriction of rat main pulmonary artery: role of endogenous channels, and phosphodiesterase inhibition. J Cardiovasc Pharmacol. 2001 Aug;38(2):325-34. Hypoxic vasoconstriction decreased by 28% (p < 0.01) in presence of the Kv,-voltage-dependent channel blocker 4-aminopyridine (10 (-3) M), whereas the other K+ channel blockers, charybdotoxin (BKCa, large-conductance Ca2+-sensitive K+ channels) and apamin (SKCa, small-conductance Ca2+-sensitive K+ channels) had no effect. |
2(0,0,0,2) | Details |
| 11301069 | Goirand F, Bardou M, Dumas J, Rochette L, Dumas M: Effects of phosphodiesterase inhibitors on hypoxic pulmonary vasoconstriction. Eur J Pharmacol. 2001 Apr 6;417(1-2):141-8. K (+) channels were inhibited by glibenclamide, charybdotoxin, apamin and 4-aminopyridine and synthase by L-N (G)-nitroarginine methyl ester (L-NAME). |
2(0,0,0,2) | Details |
| 15589969 | Lo YC, Tsou HH, Lin RJ, Wu DC, Wu BN, Lin YT, Chen IJ: Endothelium-dependent and -independent vasorelaxation by a derivative MCPT: roles of cyclic nucleotides, potassium channel opening and phosphodiesterase inhibition. Life Sci. 2005 Jan 7;76(8):931-44. This relaxation was also reduced by the presence of synthase inhibitor Nomega-nitro- methylester (L-NAME, 100 microM), soluble guanylyl cyclase (sGC) inhibitors methylene blue (10 microM), 1 H-[1,2,4] oxidazolol [4,3-a] quinoxalin-1-one (ODQ, 1 microM), adenylyl cyclase (AC) blocker SQ 22536 (100 microM), ATP-sensitive K+ channel blocker (KATP) glibenclamide (1 microM), a Ca2+ activated K+ channels blocker tetraethylammonium (TEA, 10 mM) and a voltage-dependent channels blocker 4-aminopyridine (4-AP, 100 microM). |
2(0,0,0,2) | Details |
| 15749740 | Gao Y, Raj JU: Parathyroid hormone-related protein-mediated responses in pulmonary arteries and veins of newborn lambs. Am J Physiol Lung Cell Mol Physiol. 2005 Jul;289(1):L60-6. Epub 2005 Mar 4. Radioimmunoassay showed that, in the presence of a general phosphodiesterase inhibitor, PTHrP caused a concentration-dependent increase in intracellular cAMP content in arteries and veins, which was largely abolished by SQ-22536. However, relaxation was attenuated by 4-aminopyridine, inhibitor of voltage-dependent channels, in both arteries and veins, and by charybdotoxin, inhibitor of -activated channels, in veins. |
1(0,0,0,1) | Details |
| 17320058 | Gotow T, Nishi T: Involvement of a Go-type G-protein coupled to guanylate cyclase in the phototransduction cascade of molluscan simple photoreceptors. Brain Res. 2007 May 4;1144:42-51. Epub 2007 Jan 26. Thus, this new cascade contrasts with the conventional phototransduction cascade mediated by the Gt-type G-protein coupled to phosphodiesterase, seen in the vertebrate photoreceptors and the above A-P-1 or Es-1 cells. The specific channel blocker, 4-aminopyridine (4-AP), and a GC inhibitor, LY-83583, both suppressed this hyperpolarizing photocurrent. |
1(0,0,0,1) | Details |
| 18251723 | Clemente CM, Araujo PV, Palheta RC Jr, Ratts ZM, Fernandes GH, Rola FH, de Oliveira RB, dos Santos AA, Magalhaes PJ: inhibits duodenal contractility via activation of the NO-K+ channel pathway. Fundam Clin Pharmacol. 2008 Feb;22(1):61-7. Phosphodiesterase type-5 (PDE5) specifically cleaves cyclic a key intracellular secondary messenger. In isolated strips pretreated with BaCl (2) (0.2 mM), 4-aminopyridine (4-AP, 3 mM), or glybenclamide (1 microM), the -induced EC (50) value was significantly increased to 32.8 (19.1-56.4), 27.1 (15.2-48.3) and 20.1 (16.4-24.7) microM, respectively. |
1(0,0,0,1) | Details |
| 12668054 | Wang SJ, Sihra TS: Opposing facilitatory and inhibitory modulation of release elicited by cAMP production in cerebrocortical nerve terminals (synaptosomes). Neuropharmacology. 2003 Apr;44(5):686-97. The adenylyl cyclase (AC) activator, forskolin, failed to have any effect on 4-aminopyridine (4-AP)-evoked release, when added alone. Given that IBMX has dual activity, antagonizing receptors as well as inhibiting cAMP phosphodiesterase, we examined the effect of a selective A (1) receptor antagonist, 8-cyclopentyl-1,3-dipropylxanthine (DPCPX) and RO20-1724, a specific phosphodiesterase inhibitor. |
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. |
1(0,0,0,1) | Details |
| 14746926 | Schrofner S, Zsombok A, Hermann A, Kerschbaum HH: decreases a -activated current via activation of phosphodiesterase 2 in Helix U-cells. Brain Res. 2004 Feb 27;999(1):98-105. KCa-current amplitude in U-cells was sensitive to Ba2+, TEA, iberiotoxin, kaliotoxin and charybdotoxin (ChTX), but not to 4-aminopyridine (4-AP) (up to 30 mM) and apamin (up to 300 nM). |
1(0,0,0,1) | Details |