Neutrophils are thought to cause tissue damage following hemorrhagic shock. The initial injury resulting from trauma can initiate a cascade of events leading to a non-specific inflammatory response. This inflammatory response results in the priming of neutrophils, which, upon activation by a secondary stimulus, release their armament of cytotoxic substances indiscriminately. This results in tissue damage away from the initial insult. The renin-angiotensin system and its major signaling molecule angiotensin II (angll) play an important role in stimulating mesenteric vasoconstriction and ischemia which is thought to be a key step in provoking the systemic inflammatory response. Evidence for a stimulatory effect of angll directly on neutrophils suggests that it might play an additional role in the inflammatory response following trauma. In this study, I planned to confirm results obtained in other labs which have implicated angll as a stimulator of ROS production and CD11b up regulation. Rat neutrophils were isolated and incubated with angll, fMLP, PMA, or losartan followed by angll. Reactive oxygen species production was quantified using dihydrorhodamine 123 oxidation to fluorescent rhodamine 123, and the effects of angll on CD11b expression were detected using FITC conjugated anti-CD11b antibodies. The mean fluorescent intensity of rhodamine 123 and FITC was measured using flow cytometry. Angiotensin II at concentrations of 500 nM, 1 nM, and 500 pM stimulated increased expression of CD11b but had no effect on ROS production. This data confirms the effect of angll on CD11b expression, but contradicts previous findings by others in regards to the effect on ROS production. Despite the lack of ROS production, stimulation of increased CD11b expression still implicates angll as a molecule capable of modulating neutrophil function (CD11b is a pivotal player in neutrophil mediated tissue damage). Combined with its established vacular effects and evidence that angll concentrations can remain elevated several days after traumatic insult, the observed CD11b elevation adds to the data suggesting that angll might be an important target for therapeutic intervention in the prevention of MODS.