Fig. 6. Modulation of strain-increased extracellular signal-regulated kinase (ERK) phosphorylation and endothelin-1 (ET-1) release by propofol, in part via nitric oxide/cyclic guanosine monophosphate (cGMP)-dependent protein kinase (PKG) pathway. ( A ) Under strain treatment, cells were incubated with propofol (30 M), S-Nitroso-N-acetylpenicillamine (SNAP) or 8-bromoguanosine-3′,5′-cyclic monophosphate (100 μm) for 30 min in the absence or presence of PTIO (nitric oxide scavenger) or KT-5823 (a specific inhibitor of PKG; 1 μm). After strain treatment, cells were lysed and the phosphorylation of ERK was determined. Data are represented as fold induction relative to control groups. Results are shown as mean ± SEM (n = 5). * P < 0.05 versus control; # P < 0.05 versus strain treatment. ( B ) PTIO or KT5823 reversed the inhibitory effect of propofol on strain-induced ET-1 release in human umbilical vein endothelial cells (HUVECs). Cells were treated with cyclic strain for 24 h in the absence or presence of propofol, or propofol plus PTIO or KT-5823. Data were presented as a percentage change of experimental groups, as compared with untreated controls. Results are shown as mean ± SEM (n = 6). * P < 0.05 versus control; # P < 0.05 versus cyclic strain.