Gene interactions and pathways from curated databases and text-mining

◀ Back to NOS1

FGFR3 — NOS1

Text-mined interactions from Literome

Choate et al., Exp Physiol 2000 : The nitric oxide synthase inhibitor N G-nitro-L-arginine ( L-NA ; 50 microM ) significantly attenuated the ACh-relaxation in control and trained animals ( P < 0.05 ) ... Inhibition of nitric oxide synthase attenuated the ACh-relaxation of rings from control and trained animals, but this effect was significantly larger in the vessels from trained animals
Pagliaro et al., Cardiovasc Res 2000 : NOS inhibition by NG-monomethyl-L-arginine ( L-NMMA ) did not alter basal flow at 40 mm Hg PP, but modestly lowered flow ( -5 %, P < 0.001 ) at higher PP ( 100 mm Hg ), reducing PP-flow augmentation by -36 %, and acetylcholine (ACh) induced flow elevation by -39 %
Støen et al., Acta Physiol Scand 2001 : Lower sensitivity to NOS inhibition and a larger increase in cGMP in response to ACh could indicate a higher efficacy of the NO/cGMP pathway in this vessel in the newborn piglet
Xu et al., Am J Physiol Heart Circ Physiol 2002 : Only NOS inhibition with L-NAME ( not ARR-17477 ) reduced ACh and ADP responses ( by 65-75 % ), which suggests that all of the NO dependence in the vasodilating actions of those agonists derived from eNOS
Thomsen et al., J Physiol 2002 (Diabetic Neuropathies) : In age matched controls, SIN-1 induced vasodilatation in the presence of TEA + L-NNA + indomethacin, basal NOS activity and the initial vasodilatory response to ACh during NOS and COX inhibition all decreased with maturation
Wang et al., Kidney Int 2003 (Hypertension...) : We contrasted acetylcholine (ACh) induced EDR, 3-morphollinosydnonimine ( SIN-1 ) -induced endothelium independent relaxation ( EIDR ) and constitutive nitric oxide synthase ( cNOS ) activity in subcutaneous resistance vessels and plasma levels and excretion of NO2-/NO3- ( NOX ) in normal, control ( N = 10 ) patients with ADPKD or essential hypertension
Hatoum et al., Am J Physiol Heart Circ Physiol 2005 : ACh markedly increased the dichlorofluorescein fluorescence in intact arterioles in the presence of nitric oxide synthase and cyclooxygenase inhibitors compared with control and compared with catalase treated microvessels ( 363.6 +/- 49, 218.8 +/- 10.6, 221.9 +/- 27.9, respectively, P < 0.05 ANOVA, n = 5 arbitrary units )
Qian et al., Vascul Pharmacol 2006 (Diabetes Mellitus, Experimental) : Acetylcholine (ACh) induced endothelium dependent relaxation ( EDR ), sodium nitroprusside ( SNP ) -induced endothelium independent relaxation ( EIR ), superoxide dismutase ( SOD ) and nitric oxide synthase (NOS) were measured in aortas isolated from non-diabetic rats and exposed to a high glucose concentration and from streptozotocin induced diabetic rats
Zecchin et al., Diabetes 2007 (Obesity) : In addition, ACh induces JAK2/IRS-1 and IRS-1/phosphatidylinositol (PI) 3-kinase associations, downstream activation of Akt/protein kinase B, endothelial cell-nitric oxide synthase ( eNOS ), and extracellular signal regulated kinase ( ERK ) -1/2 ... The pharmacological blockade of JAK2 or PI 3-kinase reduced ACh stimulated eNOS phosphorylation, NOS activity, and aorta relaxation
Dawson et al., Am J Physiol Heart Circ Physiol 2008 (Myocardial Infarction) : The nNOS transduced group had significantly increased right atrial [ 3H ] ACh release, right atrial NOS activity, cGMP levels, and decreased cAMP levels
Roszer et al., Cell Tissue Res 2009 : However, few comparative studies have been performed on the role of ACh on NOS activity in non-mammalian animals
Shih et al., J Biomed Sci 2009 : Contractions of the uterus were induced with acetylcholine (Ach) ( 1 microM ), PGF2alpha ( 0.1 microM ), oxytocin ( 10-3 U/ml ), KCl ( 56.3 mM ), tetraethylammonium ( TEA ; 1 and 10 mM ), 4-aminopyridine ( 4-AP ; 5 mM ), glipizide ( 30 microM ), a nitric oxide synthase (NOS) inhibitor ( LNNA ; 10-3M ), a beta-receptor blocker ( propranolol ; 10 microM ), and a cyclooxygenase inhibitor ( indomethacin ; 60 microM )
Cervantes-Pérez et al., Pharmacol Rep 2010 (Aortic Coarctation...) : However, the ACh induced release of NO as well as NOS activity and expression were reduced in the arteries of AoCo-V rats
Beleznai et al., Cardiovasc Res 2011 (Aortic Diseases...) : Inhibition of nitric oxide ( NO ) synthase blocked ACh responses, but had no effect on maximum dilation to SLIGRL
Qian et al., Indian J Pharmacol 2012 : The thoracic aorta of male Sprague-Dawley rats was isolated to mount in the organ bath system and the effect of BA on acetylcholine (ACh) induced EDR, nitric oxide ( NO ) level, reactive oxygen species ( ROS ) level, nitric oxide synthase (NOS) activity, and superoxide dismutase ( SOD ) activity of aortic rings exposed to pyrogallol ( 500 µM ) for 15 min were measured
Leonard et al., Neuroreport 1995 : This study tested the hypothesis that inhibition of nitric oxide synthase (NOS) in the medial pontine reticular formation ( mPRF ) would cause decreased acetylcholine (ACh) release
Sandor et al., Brain Res Bull 1995 : The effect of the nitric oxide synthase inhibitor N-nitro-L-arginine methyl ester ( L-NAME ) on the basal and stimulation evoked release of dopamine ( DA ) and acetylcholine (ACh) was investigated in rat striatum
Leonard et al., J Neurosci 1997 : Local NOS inhibition by microdialysis delivery of N ( G ) -nitro-L-arginine ( NLA ) significantly reduced ACh release in the cholinergic cell body region of the pedunculopontine tegmental nucleus and in the cholinoceptive mPRF