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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