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FGFR3 — NOS3
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
Pelligrino et al., Biochem Biophys Res Commun 2000
:
Under anesthesia, using intravital microscopy and a closed cranial window system, pial arteriolar diameter changes were monitored during sequential cortical suffusions of an
eNOS dependent dilator
[acetylcholine (ACh) ] and a direct NO donor [S-nitrosoacetylpenicillamine (SNAP) ]
Buchholzer et al., Neurochem Res 2003
:
The present microdialysis study investigated a possible
role of NO and of
endothelial NO synthase (eNOS) activity in the control of hippocampal
acetylcholine (ACh) release
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
Kagota et al., J Cardiovasc Pharmacol 2004
:
In contrast, in the LPS repeated group, the SNP induced relaxation and sGC protein expression significantly decreased, while the
ACh induced relaxation and
eNOS protein expression significantly increased compared with the non treated control
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 )
Gonzalez et al., Endocrinology 2004
:
Moreover, 16K-PRL inhibited
eNOS activation
induced by
ACh , and this action resulted in the inhibition of both ACh evoked relaxation of coronary vessels in isolated perfused rat hearts and ACh induced, endothelium dependent relaxation of rat aortic segments
Sánchez et al., Am J Physiol Heart Circ Physiol 2006
:
ACh and platelet activating factor (PAF)
lead to
endothelial NO synthase (eNOS) phosphorylation and NO release ... We suggest that PAF induced eNOS translocation preferentially to cytosol reflects a differential signaling mechanism related to changes in permeability, whereas
ACh induced
eNOS translocation to the TGN is related to vasodilation
Blanco-Rivero et al., J Endocrinol 2007
:
These results show that endogenous male sex hormone deprivation does not affect the
eNOS expression or the endothelial NO release
induced by
ACh , but does decrease the vasodilator action of ACh, by increasing NO metabolism and TXA ( 2 ) formation
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
Bauer et al., Cardiovasc Res 2010
:
Acetylcholine (ACh) stimulated activation of
eNOS and agonist-driven calcium transients in endothelial cells were inhibited by TSP1
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
Adapala et al., Am J Physiol Heart Circ Physiol 2011
(Calcium Signaling) :
Here, we show that
ACh induced calcium influx and
endothelial nitric oxide synthase (eNOS) phosphorylation but not calcium release from intracellular stores is inhibited by a specific TRPV4 antagonist, AB-159908
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
Trott et al., Eur J Appl Physiol 2013
:
Stimulation with
ACh or flow
increased phosphorylation of
eNOS on ser ( 1177 ) in young ( not old ) SFA ... Preincubation of young SFA with LY-294002, abolished the
ACh induced phosphorylation of
eNOS in young SFA
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