| 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 | sodium azide |
|---|---|
| CAS | sodium azide |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 18022387 | Russo I, Del Mese P, Viretto M, Doronzo G, Mattiello L, Trovati M, Anfossi G: Sodium azide, a bacteriostatic preservative contained in commercially available laboratory reagents, influences the responses of human platelets via the /PKG/VASP pathway. Clin Biochem. 2008 Mar;41(4-5):343-9. Epub 2007 Nov 7. OBJECTIVE: The bacteriostatic preservative sodium azide (NaN (3)) activates soluble guanylate cyclase (sGC) in vascular tissues, thus elevating cellular 3',5'-cyclic guanosine monophosphate |
81(1,1,1,1) | Details |
| 8719811 | Mian KB, Martin W: The inhibitory effect of 3-amino-1,2,4-triazole on relaxation induced by and sodium azide but not peroxide or glyceryl trinitrate in rat aorta. Br J Pharmacol. 1995 Dec;116(8):3302-8. Pretreatment of endothelium-denuded rings with methylene blue (MeB, 30 microM) inhibited relaxation induced by peroxide (10 microM-1 mM), sodium azide (1-300 nM), (1-300 nM) and glyceryl trinitrate (1-100 nM) suggesting that each acted by stimulation of soluble guanylate cyclase. 5. |
32(0,1,1,2) | Details |
| 16770322 | Shahidullah M, Delamere NA: NO donors inhibit Na,K-ATPase activity by a protein kinase G-dependent mechanism in the nonpigmented ciliary epithelium of the porcine eye. Br J Pharmacol. 2006 Jul;148(6):871-80. Epub 2006 Jun 12. The inhibitory effect of SNP or sodium azide on Na,K-ATPase activity was suppressed by soluble guanylate cyclase (sGC) inhibitors, ODQ (10 microM) or methylene blue (10 microM). 6. |
31(0,1,1,1) | Details |
| 17409704 | Iwatani Y, Numa H, Atagi S, Takayama F, Mio M, Kawasaki H: [Mechanisms underlying enhanced vasodilator responses to various vasodilator agents following endothelium removal in rat mesenteric resistance arteries]. Yakugaku Zasshi. 2007 Apr;127(4):729-33. In preparations with intact endothelium and active tone, 5-min perfusion of sodium azide (non-specific guanylate cyclase (GC) activator), ANP (membrane-linked GC activator), and 8-Br- analogue) caused a concentration-dependent vasodilation that was markedly augmented by endothelium removal. |
31(0,1,1,1) | Details |
| 9347476 | Sano I, Mizumoto A, Sakai T, Tamura T, Itoh Z: Sodium azide induces relaxation of the canine gastric body by activating a guanylate cyclase-dependent pathway. Neurogastroenterol Motil. 1997 Sep;9(3):193-201. |
6(0,0,1,1) | Details |
| 8537640 | Mehdizadeh S, O'Farrell A, Bitensky L, Weisz J, Alaghband-Zadeh J, Chayen J: Histochemistry of guanylate cyclase activity. J Histochem Cytochem. 1995 Dec;43(12):1235-40. |
3(0,0,0,3) | Details |
| 8605161 | Stone JR, Sands RH, Dunham WR, Marletta MA: Spectral and ligand-binding properties of an unusual hemoprotein, the ferric form of soluble guanylate cyclase. Biochemistry. 1996 Mar 12;35(10):3258-62. |
2(0,0,0,2) | Details |
| 15563529 | Swafford AN Jr, Bratz IN, Knudson JD, Rogers PA, Timmerman JM, Tune JD, Dick GM: C-reactive protein does not relax vascular smooth muscle: effects mediated by sodium azide in commercially available preparations. Am J Physiol Heart Circ Physiol. 2005 Apr;288(4):H1786-95. Epub 2004 Nov 24. NaN (3) elicited the same cardiovascular effects as CRP preparations at equal concentrations, and its actions were blocked by inhibition of guanylate cyclase and K (+) channels. |
1(0,0,0,1) | Details |
| 7694754 | Scott TR, Bennett MR: The effect of on the efficacy of synaptic transmission through the chick ciliary ganglion. Br J Pharmacol. 1993 Oct;110(2):627-32. These results suggest that modulates synaptic transmission through the ganglion by acting on an endogenous guanylate cyclase that produces cyclic GMP. Sodium azide (100 microM), shown in sympathetic ganglia to stimulate production of cyclic GMP, did not modulate synaptic efficacy significantly. 3. 8-Br-cyclic-GMP (100 microM) increased synaptic efficacy by an average 61%. |
1(0,0,0,1) | Details |
| 16568613 | Iakovenko IN, Zhirnov VV: [Sodium azide as indirect donor: researches on the rat aorta isolated segments]. Ukr Biokhim Zh. 2005 Jul-Aug;77(4):120-3. The value of vasodilatation, caused by NaN3, was also decreased in the presence of soluble guanylate cyclase inhibitor ODQ (10 (-5) M). |
1(0,0,0,1) | Details |
| 8537639 | Mehdizadeh S, O'Farrell A, Bitensky L, Weisz J, Alaghband-Zadeh J, Chayen J: Measurement of synthase activity in sections of rat liver. . J Histochem Cytochem. 1995 Dec;43(12):1229-33. We found that this was correct provided that the concentration of the colloid stabilizer in the reaction medium was decreased to just below the concentration required to fully stabilize the guanylate cyclase activity in the sections. |
1(0,0,0,1) | Details |
| 11790383 | Shahidullah M, Duncan A, Strachan PD, Rafique KM, Ball SL, McPate MJ, Nelli S, Martin W: Role of catalase in the smooth muscle relaxant actions of sodium azide and cyanamide. Eur J Pharmacol. 2002 Jan 18;435(1):93-101. |
0(0,0,0,0) | Details |
| 8532139 | Stout AK, Woodward JJ: Mechanism for nitric oxide's enhancement of -stimulated [3H] release from rat hippocampal slices. Neuropharmacology. 1995 Jul;34(7):723-9. Similar to NO, the metabolic inhibitors sodium azide (NaN3, 0.1-3 mM), (KCN, 0.1-3 mM), and 2,4-dinitrophenol (2,4-DNP, 10-300 microM) also dose-dependently enhanced -stimulated [3H] NA release. |
0(0,0,0,0) | Details |
| 15711584 | Shahidullah M, Yap M, To CH: Cyclic GMP, sodium nitroprusside and sodium azide reduce aqueous humour formation in the isolated arterially perfused pig eye. Br J Pharmacol. 2005 May;145(1):84-92. |
0(0,0,0,0) | Details |
| 15683745 | Gabra BH, Afify EA, Daabees TT, Abou Zeit-Har MS: The role of the NO/ pathways in the development of morphine withdrawal induced by naloxone in vitro. Pharmacol Res. 2005 Apr;51(4):319-27. In addition, the NO precursor (5x10 (-4) M) as well as the NO donors sodium nitroprusside (SNP; 1 microM) and sodium azide (NaZ; 10 microM) were able to revert the effect of L-NAME returning the amplitude of naloxone-induced contracture to the same level in control morphine-dependent ilea. |
0(0,0,0,0) | Details |
| 19542485 | Mink SN, Jacobs H, Cheng ZQ, Kasian K, Santos-Martinez LE, Light RB: Lysozyme, a mediator of sepsis that intrinsically generates peroxide to cause cardiovascular dysfunction. Am J Physiol Heart Circ Physiol. 2009 Sep;297(3):H930-48. Epub 2009 Jun 19. We found that Lzm-S could generate H (2) O (2) and, furthermore, that this generation could be attenuated by the singlet quencher sodium azide. |
0(0,0,0,0) | Details |
| 9718094 | VanUffelen BE, Van der Zee J, de Koster BM, VanSteveninck J, Elferink JG: Sodium azide enhances neutrophil migration and exocytosis: involvement of cyclic GMP and Life Sci. 1998;63(8):645-57. |
0(0,0,0,0) | Details |