Recent results from our laboratory demonstrated that intracerebroventricular (icv) injection of hydrogen peroxide (H2O2), a reactive oxygen species, reduced water intake and pressor responses induced by icv injection of angiotensin II (Lauar et.al., 2008). Thus, in the present study we investigated the effects of icv injection of H2O2 or ATZ (3-amino-1,2,4-triazole, a catalase inhibitor) on the pressor responses induced by icv injection of the cholinergic agonist carbachol. Male Holtzman rats (280-320 g, n=8/group) were anesthetized with ketamine (80 mg/kg of body weight) combine with xylazine (7 mg/kg of body weight) and had stainless steel cannulas implanted in the lateral ventricle (LV). Mean arterial pressure (MAP) and heart rate (HR) were recorded in unanesthetized freely moving rats. A polyethylene tubing (PE-10 connected to a PE-50) was inserted into the abdominal aorta through the femoral artery on the day before the experiments under ketamine + xylazine anesthesia. MAP and HR were continuously recorded and H2O2 (5 μmol/1 μl) or PBS (vehicle, 1 μl) was injected into the LV 1 min before the injection of carbachol (4 nmol/1 µl) also into the LV, and ATZ (5 nmol/1 μl) or saline was injected into the LV 10 min before the injection of carbachol. The previous icv injection of H2O2 or ATZ reduced the pressor responses produced by icv injection of carbachol (12 ± 4 and 13 ± 4 mmHg, respectively, vs. vehicle or saline: 25 ± 4 and 30 ± 4 mmHg, respectively). No significant change on HR was produced by carbachol alone (-13 ± 13 and -31 ± 15 bpm, respectively) or combined with H2O2 or ATZ (-3 ± 9 and -8 ± 17 bpm), compared with vehicle or saline (-2 ± 16 and 13 ± 13 bpm, respectively). The results show that central injections of H2O2 or ATZ reduced the pressor response induced by icv injection of carbachol, suggesting that exogenous or endogenous H2O2 may inhibit central pressor mechanisms activated by central cholinergic activation.