@entity3957 is involved in @entity619 -induced @entity101 in XXXX .

@entity3958 @entity462 @entity101 @entity4059 @entity3959 @entity619 @entity1617 @entity842 @entity460 @entity972 @entity35 @entity3352 @entity3957 @entity60372 @entity934
Glucocorticoid (GC)-induced @entity101 is a common clinical problem still poorly understood. The presence of GC receptor (GR) in vascular smooth muscle and endothelial cells suggests a direct role for GC in vasculature. In response to hemodynamic shear stress, endothelium tonically releases @entity842 (NO), @entity4059 ( @entity4059 ) and prostacyclin contributing to vascular homeostasis. Recently, @entity3957 ( @entity3958 ) has been proposed as a candidate for @entity4059 . @entity3958 is endogenously mainly formed from @entity462 by the action of @entity3959 -b-synthase (CBS) and @entity3959 -y-lyase (CSE). It plays many physiological roles and contributes to cardiovascular function. Here we have evaluated the role played by @entity3958 in mesenteric arterial bed and in carotid artery harvested from @entity35 treated with vehicle or @entity619 (DEX; 1.5   mg/kg/day) for 8 days. During treatments systolic blood pressure was significantly increased in conscious @entity35 . @entity4059 contribution was evaluated in ex-vivo by performing a concentration-response curve induced by @entity934 ( @entity1617 ) in presence of a combination of @entity3352 and L-NG-Nitroarginine methyl ester in both vascular districts. @entity4059 -mediated relaxation was significantly reduced in DEX-treated group in both mesenteric bed and carotid artery. @entity4059 -mediated relaxation was abolished by pre-treatment with both apamin and charybdotoxin, inhibitors of small and big @entity460 -dependent @entity972 channels respectively, or with @entity60372 , inhibitor of CSE. Western blot analysis revealed a marked reduction in CBS and CSE expression as well as @entity3958 production in homogenates of mesenteric arterial bed and carotid artery from DEX-treated @entity35 . In parallel, @entity3958 plasma levels were significantly reduced in DEX group compared with vehicle. In conclusion, an impairment in @entity4059 / @entity3958 signaling occurs in earlier state of GC-induced @entity101 in @entity35 suggesting that counteracting this dysfunction may be beneficial to manage DEX-associated increase in blood pressure.
