Rapid nontranscriptional activation of endothelial nitric oxide synthase mediates increased cerebral blood flow and stroke protection by corticosteroids
J. Clin. Invest. Florian P. Limbourg, et al. 110:1729 doi:10.1172/JCI15481 [Go to this article.]

Figure 5
Nontranscriptional activation of eNOS by high-dose corticosteroids. (a) Shown are cGMP levels in human ECs after dexamethasone treatment. The upper panel shows cGMP levels in HUVECs stimulated with S-nitrosoglutathione (GSNO, 300 μM) or dexamethasone (100 nM) with or without LY294002 (LY, 30 μM) or L-NAME (1 mM, n = 4). The lower panel shows cGMP levels in HAECs stimulated with dexamethasone with or without LY294002 (n = 4). Ctrl, control. *P < 0.05 vs. control. GSNO, S-nitrosoglutathione; LY, LY294002. (b) Effects of 100 nM of dexamethasone, prednisolone, hydrocortisone, or triamcinolone acetonide on eNOS activity in HUVECs (n = 2). Pred, prednisolone; HC, hydrocortisone; TA, triamcinolone acetonide. (c) Dose–response effects of dexamethasone on eNOS activity (HUVECs, n = 5) and GRE-luciferase activity (bovine aortic endothelial cells transfected with pGRE-luc, n = 6). *P < 0.01 vs. control. (d) Dexamethasone serum levels in mice after intraperitoneal bolus administration of low- and high-dose dexamethasone.