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FGFR3 — SOD3
Text-mined interactions from Literome
Münzel et al., Br J Pharmacol 1999
:
Pretreatment ( 1 h ) of vessels with diethyldithiocarbamate ( DETC ; 10 mM ) attenuated vasorelaxant responses to GTN and
ACh , increased vascular *O2- production, and
inhibited SOD activity in vessel homogenates to a similar degree as observed in in vivo tolerance
Maczewski et al., J Mol Cell Cardiol 2000
(Myocardial Ischemia) :
SOD , but not bosentan, partially
prevented the effect of PMA on the
ACh response
Ammar et al., Cardiovasc Res 2000
(Diabetes Mellitus, Experimental) :
Changes in coronary microvascular diameters in diabetic ( blood glucose > 200 mg % ) and normal animals to
ACh ( 1-100 microM, topically ) in the
presence and absence of
superoxide dismutase and catalase were measured using intravital microscopy coupled to stroboscopic epi-illumination and jet ventilation
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
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