| Name | guanylate cyclase |
|---|---|
| Synonyms | AMDM; Natriuretic peptide receptor; ANP B; ANPRB; Atrial natriuretic peptide B type receptor; Atrial natriuretic peptide receptor B; Atrial natriuretic peptide receptor B precursor (ANP B) (ANPRB) (GC B) (Guanylate cyclase B); Atrionatriuretic peptide receptor B… |
| Name | 4-aminopyridine |
|---|---|
| CAS | 4-pyridinamine |
| PubMed | Abstract | RScore(About this table) | |
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| 16917023 | Agren P, Cogolludo AL, Kessels CG, Perez-Vizcaino F, De Mey JG, Blanco CE, Villamor E: Ontogeny of chicken ductus arteriosus response to and vasoconstrictors. Am J Physiol Regul Integr Comp Physiol. 2007 Jan;292(1):R485-96. Epub 2006 Aug 17. On embryonic day 15, the chicken DA did not respond to O (2) (0 to 21%), (NE), or but contracted in response to high-K (+) solution, the inhibitor of voltage-gated channels 4-aminopyridine, U-46619, and endothelin (ET)-1. -induced contraction was restricted to the pulmonary side of the DA and was augmented by the synthase inhibitor N (omega)-nitro- methyl ester and the soluble guanylate cyclase inhibitor 1H-[1,2,4] oxadiazolo [4,3-a] quinoxalin-1-one and reduced by the peptidic ET (A) and ET (B)-receptor antagonist PD-142,893. |
1(0,0,0,1) | Details |
| 15028525 | Corti A, Mannarino C, Mazza R, Angelone T, Longhi R, Tota B: Chromogranin A N-terminal fragments vasostatin-1 and the synthetic CGA 7-57 peptide act as cardiostatins on the isolated working frog heart. Gen Comp Endocrinol. 2004 Apr;136(2):217-24. This vasostatin response was unaffected by pretreatment with either Triton X-100 or two synthase inhibitors, i.e., N (G)-monomethyl- and L-N5 (5)(1-iminoethyl) or the soluble guanylate cyclase inhibitor 1H-(1,2,4) oxadiazolo-(4,3-a) quinoxalin-1-one, indicating an endocardial endothelium---independent mechanism. On the contrary, it was dependent from both extracellular Ca (2+) and K (+) channels, since it was abolished by pretreatment to either the Ca (2+) channel inhibitors lanthanum and or the K (+) channel inhibitors Ba (2+), 4-aminopyridine, tetraethylammonium and glibenclamide. |
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| 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. Accordingly, the guanylate cyclase inhibitors 1H-[1,2,4]-oxadiazole-[4,3-a]-quinoxalin-1-one (ODQ, 10 microM) and 4H-8-bromo-1,2,4-oxadiazolo (3,4-d) benz (b)(1,4) oxazin-1-one (NS 2028, 10 microM) almost abolished relaxations to EFS and Angeli's salt. 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]. |
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| 12548092 | Andre E, Malheiros A, Cechinel-Filho V, Yunes RA, Calixto JB: Role of and K+ channels in relaxation induced by polygodial in rabbit corpus cavernosum in vitro. J Cardiovasc Pharmacol. 2003 Feb;41(2):300-6. The (NO) synthase inhibitor L-NOARG and the guanylate cyclase inhibitors LY 83583 and ODQ markedly inhibited the relaxation induced by polygodial (% of inhibition of 79, 48, and 51, respectively) and those caused by (% of inhibition of 100, 49, and 32, respectively). In contrast, apamin, charybdotoxin, and 4-aminopyridine or the protein kinase A inhibitor KT 5720 all failed to affect either polygodial or -mediated relaxation in these preparations. |
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| 18533147 | El-Mas MM, El-Gowilly SM, Gohar EY, Ghazal AR: Pharmacological characterization of cellular mechanisms of the renal vasodilatory effect of in rats. Eur J Pharmacol. 2008 Jul 7;588(2-3):294-300. Epub 2008 Apr 30. Chemical denudation of the endothelium with 3-[(3-cholamidopropyl)-dimethyl-ammonio]-1-propane-sulfonate (CHAPS), or inhibition of NOS (NG-nitro- L-NNA), or guanylate cyclase (methylene blue) almost abolished the renal vasodilatory action of vasodilation was also significantly attenuated after selective blockade of ATP-sensitive (K (ATP), glibenclamide) or inward rectifier (Kir, BaCl2) K+ channels but remained unaltered after blockade of large-conductance -activated (BKCa, tetraethylammonium, TEA) or voltage-dependent (Kv, 4-aminopyridine) K+ channels. |
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| 19268563 | Crestani S, Rattmann YD, Cipriani TR, de Souza LM, Iacomini M, Kassuya CA, Marques MC, da Silva-Santos JE: A potent and -dependent hypotensive effect induced in rats by semi-purified fractions from Maytenus ilicifolia. Vascul Pharmacol. 2009 Jul;51(1):57-63. Epub 2009 Mar 4. Our results demonstrate that preparations obtained from M. ilicifolia present a potent hypotensive effect in vivo, an event predominantly dependent on the nitricoxide/guanylate cyclase pathway. The hypotension induced by EAF was circumvented by L-NAME, methylene blue andODQ, strongly reduced by tetraethylammonium and 4-aminopyridine (but not by glibenclamide), and abolished by association of these three potassium channel blockers. |
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| 10781427 | Halla TR, Madden JA, Gordon JB: Mediators of alkalosis-induced relaxation of piglet pulmonary veins. Am J Physiol Lung Cell Mol Physiol. 2000 May;278(5):L968-73. This relaxation was significantly blunted in rings without functional endothelium and in rings treated with synthase or guanylate cyclase inhibitors. |
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| 10742286 | Selemidis S, Cocks TM: Nitrergic relaxation of the mouse gastric fundus is mediated by cyclic GMP-dependent and ryanodine-sensitive mechanisms. Br J Pharmacol. 2000 Apr;129(7):1315-22. Apamin (1 microM), charybdotoxin (0.1 microM), iberiotoxin (0.1 microM), tetraethylammonium (TEA; 1 mM), glibenclamide (10 microM) and 4-aminopyridine (1 mM) had no effect on either NANC- or SNP-evoked relaxations, the latter of which were also unaffected by high extracellular K (+) (68 mM). 4. |
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| 20361315 | Ahn SW, Kim SH, Kim JH, Choi S, Yeum CH, Wie HW, Sun JM, So I, Jun JY: Phentolamine inhibits the pacemaker activity of mouse interstitial cells of Cajal by activating ATP-sensitive K+ channels. Arch Pharm Res. 2010 Mar;33(3):479-89. Epub 2010 Mar 30. Phentolamine-induced effects on the pacemaker currents and the pacemaker potentials were significantly inhibited by ATP sensitive K (+) channel blocker glibenclamide, but not by TEA, apamin, or 4-aminopyridine. |
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| 19919833 | Dhaese I, Van Colen I, Lefebvre RA: Mechanisms of action of in relaxation of mouse distal colonic smooth muscle. Eur J Pharmacol. 2010 Feb 25;628(1-3):179-86. Epub 2009 Nov 15. The NaHS-induced relaxation was not influenced by the K (+) channels blockers glibenclamide, apamin, charybdotoxin, barium and 4-aminopyridine. |
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| 16243464 | Rattmann YD, Cipriani TR, Sassaki GL, Iacomini M, Rieck L, Marques MC, da Silva-Santos JE: -dependent vasorelaxation induced by extractive solutions and fractions of Maytenus ilicifolia Mart ex Reissek (Celastraceae) leaves. J Ethnopharmacol. 2006 Apr 6;104(3):328-35. Epub 2005 Oct 21. Further, relaxation induced by this ethanolic supernatant have been strongly inhibited by the guanylate cyclase inhibitors methylene blue and ODQ, as well as by the potassium channel blockers 4-aminopyridine and tetraethylammonium, but was unchanged by the cyclooxygenase inhibitor indomethacin and the membrane receptor antagonists atropine, HOE-140 and pirilamine. |
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| 12684264 | Gao YJ, Hirota S, Zhang DW, Janssen LJ, Lee RM: Mechanisms of -peroxide-induced biphasic response in rat mesenteric artery. Br J Pharmacol. 2003 Mar;138(6):1085-92. In summary, in PHE-precontracted rat mesenteric artery: (1) the response to H (2) O (2) shifted qualitatively from contraction to a biphasic response as H (2) O (2) increased to 0.3 mM or higher; (2) the relaxation response is caused by the activation of K (+) channels, with voltage-dependent K (+) channels playing a primary role; and the contraction is likely to be mediated by A (2); (3) the K (+) channel activation by H (2) O (2) is independent of phospholipase A (2), cyclooxygenase, lipoxygenase, cytochrome P450 monooxygenase, or guanylate cyclase. KCl at 40 mM inhibited the relaxation response to H (2) O (2) by 98+/-24%. 4-Aminopyridine (4-AP) inhibited while tetraethylammonium (TEA), charybdotoxin, or glibenclamide attenuated the relaxation response. |
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| 20164203 | Flinsenberg TW, Van der Sterren S, van Cleef AN, Schuurman MJ, Agren P, Villamor E: Effects of gender and on chicken ductus arteriosus reactivity. Am J Physiol Regul Integr Comp Physiol. 2010 Feb 17. In vitro contractions (assessed with a wire myograph) induced by normoxia, KCl, 4-aminopyridine, U46619, or endothelin-1 as well as relaxations induced by sodium nitroprusside, BAY 41-2272, isoproterenol, forskolin,Y-27632, and hydroxyfasudil were not significantly different between males and females. |
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| 18223671 | Hernandez M, Barahona MV, Recio P, Navarro-Dorado J, Bustamante S, Benedito S, Garcia-Sacristan A, Prieto D, Orensanz LM: Role of neuronal voltage-gated K (+) channels in the modulation of the nitrergic neurotransmission of the pig urinary bladder neck. Br J Pharmacol. 2008 Mar;153(6):1251-8. Epub 2008 Jan 28. The voltage-gated K (+) (Kv) channels inhibitor 4-aminopyridine, greatly enhanced the nitrergic relaxations evoked by EFS, but did not affect the NaNO (2) solution-induced relaxations. |
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| 18045622 | Wang Y, Shi JG, Wang MZ, Che CT, Yeung JH: Mechanisms of the vasorelaxant effect of 1, 5-dihydroxy-2, 3-dimethoxy-xanthone, an active metabolite of 1--2, 3, 5-trimethoxy-xanthone isolated from a Tibetan herb, Halenia elliptica, on rat coronary artery. Life Sci. 2008 Jan 2;82(1-2):91-8. Epub 2007 Nov 1. In endothelium-denuded coronary artery rings, the vasorelaxant effect of HM-5 was inhibited by a potassium channel blocker, TEA (10 mM), and 4-aminopyridine (4-AP, a K (v) blocker; 1 mM) but not by other K+ channel blockers such as iberiotoxin (100 nM), barium (100 microM) and glibenclamide (10 microM). |
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| 11284450 | Tanaka Y, Mitani A, Igarashi T, Someya S, Otsuka K, Imai T, Yamaki F, Tanaka H, Saitoh M, Nakazawa T, Noguchi K, Hashimoto K, Shigenobu K: HNS-32, a novel azulene-1-carboxamidine derivative, inhibits nifedipine-sensitive and -insensitive contraction of the isolated rabbit aorta. Naunyn Schmiedebergs Arch Pharmacol. 2001 Mar;363(3):344-52. Relaxation elicited by HNS-32 was not affected by the adenylate cyclase inhibitor, 9-(tetrahydro-2'-furyl) (SQ 22,536, 10 (-4) M), the soluble guanylate cyclase inhibitor, 1H-(1,2,4)-oxadiazolo-(4,3-a)-quinoxalin-1-one (ODQ, 10 (-5) M) or a cocktail of K+ channel blockers (glybenclamide 10 (-6) M, tetraethylammonium 2x10 (-3) M, apamin 10 (-7) M, 4-aminopyridine 10 (-4) M and Ba2+ 10 (-5) M). |
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| 15474532 | Imbrogno S, Angelone T, Corti A, Adamo C, Helle KB, Tota B: Influence of vasostatins, the chromogranin A-derived peptides, on the working heart of the eel (Anguilla anguilla): negative inotropy and mechanism of action. Gen Comp Endocrinol. 2004 Oct;139(1):20-8. The VS-1-mediated negative inotropism was abolished by exposure to inhibitors of either Gi/o protein (pertussis toxin; PTx) or M1 muscarinic receptors (Pirenzepine) or (Lantanum and and (Ba2+, 4-aminopyridine, tetraethylammonium, glibenclamide) channels, while it required an intact endocardial endothelium (EE). |
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| 12020933 | Testai L, Chericoni S, Calderone V, Nencioni G, Nieri P, Morelli I, Martinotti E: Cardiovascular effects of Urtica dioica L. (Urticaceae) roots extracts: in vitro and in vivo pharmacological studies. J Ethnopharmacol. 2002 Jun;81(1):105-9. Furthermore, potassium channel blockers (TEA, 4-aminopyridine, quinine, but not glybenclamide) antagonized the vasodilator action of the purified fraction F1W of U. dioica. |
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| 15993634 | Costa RS, Assreuy J: Multiple channels mediate -induced inhibition of rat vascular smooth muscle cell proliferation. Nitric Oxide. 2005 Sep;13(2):145-51. In this report, we show that tetraethylammonium (TEA, a non-selective blocker of KC, 300 microM), and 4-aminopyridine (a selective blocker of voltage-dependent KC, 100 microM) prevented SNAP inhibitory effects on cell proliferation, whereas glibenclamide (a selective blocker of ATP-dependent KC, 1 microM) was ineffective. |
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| 15237094 | Wu BN, Lin RJ, Lo YC, Shen KP, Wang CC, Lin YT, Chen IJ: KMUP-1, a derivative, induces relaxation of guinea-pig isolated trachea: the role of the epithelium, cyclic nucleotides and K+ channels. Br J Pharmacol. 2004 Aug;142(7):1105-14. Epub 2004 Jul 5. Tracheal relaxation induced by KMUP-1 was attenuated by epithelium removal and by pretreatment with inhibitors of soluble guanylate cyclase (sGC) (1H-[1,2,4] oxadiazolo [4,3-a] quinoxalin-1-one (ODQ), 1 microm), synthase (Nomega-nitro- methyl ester, 100 microm), K+ channels (tetraethylammonium, 10 mm), KATP channels (glibenclamide, 1 microm), voltage-dependent K+ channels (4-aminopyridine, 100 microm) and Ca2+-dependent K+ channels (charybdotoxin, 0.1 microm or apamin, 1 microm). |
31(0,1,1,1) | Details |
| 19338582 | Andrews KL, Irvine JC, Tare M, Apostolopoulos J, Favaloro JL, Triggle CR, Kemp-Harper BK: A role for (HNO) as an endothelium-derived relaxing and hyperpolarizing factor in resistance arteries. Br J Pharmacol. 2009 Jun;157(4):540-50. Epub 2009 Mar 26. KEY RESULTS: Vasorelaxation to the HNO donor, Angeli's salt, was attenuated in both species by the soluble guanylate cyclase inhibitor (ODQ, 1H-[1,2,4] oxadiazolo [4,3-a] quinoxaline-1-one), the voltage-dependent K (+) channel inhibitor, 4-aminopyridine (4-AP) and the HNO scavenger, |
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| 12642395 | Andrews KL, McGuire JJ, Triggle CR: A photosensitive vascular smooth muscle store of in mouse aorta: no dependence on expression of endothelial nitric oxide synthase. Br J Pharmacol. 2003 Mar;138(5):932-40. Equal levels of photorelaxation (45+/-2%; n=34) was observed in both strains. (3) 1H-[1,2,4]-oxadiazolo [4,3-a] quinoxalin-1-one (ODQ), K (+), 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (c-PTIO), 4-aminopyridine (4-AP) and ethacrynic acid significantly reduced the photorelaxation response. |
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| 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 (+). |
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| 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. The specific channel blocker, 4-aminopyridine (4-AP), and a GC inhibitor, LY-83583, both suppressed this hyperpolarizing photocurrent. |
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| 12079001 | Paulino N, Scremin FM, Raichaski LB, Marcucci MC, Scremin A, Calixto JB: Mechanisms involved in the relaxant action of the ethanolic extract of propolis in the guinea-pig trachea in-vitro. J Pharm Pharmacol. 2002 Jun;54(6):845-52. Finally, the propolis extract-induced relaxation was inhibited by the synthase inhibitor L-N (G)-nitroarginine (L-NOArg, 100 microM) (48+/-6%), and by the soluble guanylatecyclase inhibitormethylene blue (10 microM) (37+/-6%), whilethe moreselectivesoluble guanylate cyclase inhibitor 1H-[1,2,4] oxadiazolol [4,3-alquinoxalin-1-one (ODQ, 1 microM) produced only a parallel (about 3 fold) rightward displacement of the propolis extract concentration-response curve. Pre-incubation of guinea-pig tracheas with tetraethylamonium (100 mM) or with 4-aminopyridine (10mM) reduced the propolis extract-induced relaxation by 31+/-10% and 28+/-2%. |
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| 16151435 | Wu BN, Tu HF, Welsh DG, Chen IJ: KMUP-1 activates BKCa channels in basilar artery myocytes via cyclic nucleotide-dependent protein kinases. Br J Pharmacol. 2005 Nov;146(6):862-71. BKCa current activation by KMUP-1 was markedly inhibited by a soluble guanylate cyclase inhibitor (ODQ 10 microM), an adenylate cyclase inhibitor (SQ 22536 10 microM), competitive antagonists of and cAMP (Rp- 100 microM and Rp-cAMP, 100 microM), and - and cAMP-dependent protein kinase inhibitors (KT5823, 300 nM and KT5720, 300 nM). |
1(0,0,0,1) | Details |
| 10832600 | Terluk MR, da Silva-Santos JE, Assreuy J: Involvement of soluble guanylate cyclase and -activated channels in the long-lasting hyporesponsiveness to induced by in rat aorta. Naunyn Schmiedebergs Arch Pharmacol. 2000 May;361(5):477-83. In contrast, 4-aminopyridine (1 mM) and glibenclamide (10 microM) had no effect. |
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| 16455108 | Leal LK, Costa MF, Pitombeira M, Barroso VM, Silveira ER, Canuto KM, Viana GS: Mechanisms underlying the relaxation induced by isokaempferide from Amburana cearensis in the guinea-pig isolated trachea. Life Sci. 2006 May 30;79(1):98-104. Epub 2006 Feb 7. The IKPF-induced relaxation was inhibited in 41% by the (NO) synthase inhibitor L-NAME (100 microM); in 31% and 50% by the soluble guanylate cyclase (sGC) inhibitor ODQ (3 and 33 microM); by (31%) and also by (37%). On the other hand, 4-aminopyridine (100 microM), a nonselective K (+) channel antagonist, did not significantly influence the effect of IKPF, while IbTX induced a rightward displacement of the IKPF concentration-response curve. |
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| 12743008 | Irvine JC, Favaloro JL, Kemp-Harper BK: NO- activates soluble guanylate cyclase and Kv channels to vasodilate resistance arteries. Hypertension. 2003 Jun;41(6):1301-7. Epub 2003 May 12. The soluble guanylate cyclase inhibitor ODQ (3 and 10 micromol/L) concentration-dependently inhibited relaxation responses to Angeli's salt (41.0+/-6.0% versus control 93.4+/-1.9% at 10 micromol/L). The voltage-dependent K+ channel inhibitor 4-aminopyridine (1 mmol/L) caused a 9-fold (P <0.01) decrease in sensitivity to Angeli's salt, whereas glibenclamide, iberiotoxin, charybdotoxin, and apamin were without effect. |
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| 18264125 | Lafayette SS, Vladimirova I, Garcez-do-Carmo L, Monteforte PT, Caricati Neto A, Jurkiewicz A: Evidence for the participation of in non-genomic relaxations induced by androgenic steroids in rat vas deferens. Br J Pharmacol. 2008 Mar;153(6):1242-50. Epub 2008 Feb 11. Relaxation to was resistant to the K (+) channel antagonists glibenclamide, 4-aminopyridine and charybdotoxin. |
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| 10719960 | Kinoshita H, Ishikawa T, Hatano Y: Role of K+ channels in augmented relaxations to sodium nitroprusside induced by mexiletine in rat aortas. Anesthesiology. 2000 Mar;92(3):813-20. Concentration-response curves of sodium nitroprusside (10 (-10) to 10 (-5) M) and 1--2-oxo-3-(N-methyl-3-aminopropyl)-3-methyl-1-triazene (NOC-7; 10 (-9) to 10 (-5) M) were obtained in the absence and in the presence of mexiletine, in combination with a soluble guanylate cyclase inhibitor, 1H-[1,2,4] oxadiazolo [4,3,-a] quinoxaline-1-one (ODQ), or inhibitors for ATP-sensitive K+ channels (glibenclamide), inward rectifier K+ channels (BaCl2), delayed rectifier K+ channels (4-aminopyridine), large conductance Ca2+-dependent K+ channels (iberiotoxin), or small conductance Ca2+-dependent K+ channels (apamin). |
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| 11030715 | Homer KL, Wanstall JC: Cyclic GMP-independent relaxation of rat pulmonary artery by a diazeniumdiolate donor. Br J Pharmacol. 2000 Oct;131(4):673-82. ODQ-resistant relaxation to (i. e. relaxation seen in the presence of 10 microM ODQ) was inhibited by (80 mM), charybdotoxin (300 nM), iberiotoxin (300 nM), apamin (100 nM), ouabain (1 mM) or thapsigargin (100 nM) but not by 4-aminopyridine (3 mM), glybenclamide (10 microM) or (10 microM). Responses to were only partially blocked by the soluble guanylate cyclase inhibitor, ODQ (1H:-[1,2,4] Oxadiazolo-[4,3,-a] quinoxalin-1-one) at concentrations up to 30 microM. |
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| 17822718 | Wang Y, Shi JG, Wang MZ, Che CT, Yeung JH: Mechanisms of the vasorelaxant effect of 1--2, 3, 5-trimethoxy-xanthone, isolated from a Tibetan herb, Halenia elliptica, on rat coronary artery. Life Sci. 2007 Sep 1;81(12):1016-23. Epub 2007 Aug 17. The endothelium-dependent effects of HM-1 was confirmed when its vasorelaxant effect was inhibited after addition of synthase (NOS) inhibitor N (omega)-nitro- methyl ester (100 microM) or the soluble guanylate cyclase inhibitor 1H-[1, 2, 4] oxadiazolo [4,3-alpha] quinoxalin-1-one (ODQ, 10 microM). In endothelium-denuded coronary artery rings, the vasorelaxant effect of HM-1 was unaffected by potassium channel blockers such as tetraethylammonium (10 mM), iberiotoxin (100 nM), barium (100 microM) and 4-aminopyridine (1 mM). |
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| 10618154 | Ghisdal P, Gomez JP, Morel N: Action of a NO donor on the excitation-contraction pathway activated by in rat superior mesenteric artery. J Physiol. 2000 Jan 1;522 Pt 1:83-96. Responses to SNAP were unaffected by the following K+ channel blockers: glibenclamide, 4-aminopyridine, apamin and charybdotoxin, and by increasing the KCl concentration to 25 mM. The guanylate cyclase inhibitor ODQ abolished the increase in cyclic GMP content evoked by SNAP and inhibited the effects of SNAP on contraction, Vm and accumulation of inositol phosphates in -stimulated artery. |
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