The role of rho kinase (ROCK) in edema-induced suppression of intestinal contractile activity is demonstrated. Panel A. Inhibition of contractile activity after treatment with rho kinase inhibitor (Y-27632, 10 uM) alone, Y-27632 treatment after pretreatment with a myosin light chain kinase inhibitor (W-7, 50 uM), and Y-27632 treatment after pretreatment with a myosin light chain phosphatase inhibitor (Okadaic acid, 250 nM). Panel B. ROCK activity towards an MYPT1 peptide substrate in intestinal smooth muscle lysates from CONTROL and EDEMA groups collected 6 hours after surgery. Panel C. rhoA GTPase activity in intestinal smooth muscle tissue lysates from CONTROL and EDEMA groups measured as rhoA-GTP binding to an immobilized effector molecule. Panel D. Representative Western blot of ROCK2 in CONTROL and EDEMA groups 6 hours after surgery. Panel E. Quantification of ROCK2 protein levels normalized to GAPDH in intestinal smooth muscle from CONTROL and EDEMA group at 6 hour time point (GAPDH, glyceraldehydes dehydrogenase). Panel F. Representative Western blot of rhoA in CONTROL and EDEMA groups 6 hours after surgery. Panel G. Quantification of rhoA protein levels normalized to GAPDH in intestinal smooth muscle from CONTROL and EDEMA group at 6 hour time point. (Panel A, n=5 per group for no pretreatment and okadaic acid pretreatment group, n=3 for W-7 pretreatment groups; Panel B, n=10 per group; Panel C, n=5 per group; Panel E, n=9 per group; Panel G, n=9 per group; *, p<0.05 vs. CONTROL)