During sepsis, there are changes in the cardiovascular system that are characterized by a drop in the blood pressure (BP), and increased heart rate (HR). It has been reported that during the septic shock the endocannabinoid system is active, and both anandamide and 2-AG endogenous endocannabinoids could act on CB1 and CB2 receptors. Moreover, the endocannabinoids, acting on CB1 receptors, are potent vasodilators and CB2 receptors modulate the immune response during sepsis. Thus, the increase in the concentration of endocannabinoids may worsen the cardiovascular and immunological response to sepsis. Thereby, we studied the cardiovascular effects of an increase in endocannabinoids by the inhibition of the FAAH (fatty acida mine hydrolase), which is the enzyme responsible by the degradation of endocannabinoids, during the septic shock induced by cecal ligation and puncture (CLP). To that, we utilized male Wistar rats. Animals were anesthetized with 2,2,2-tribromoethanol (250 mg/kg i.p., Sigma-Aldrich, St. Louis, MO, USA) and had a radio-telemetry probe implanted into the descendent aorta, to measure cardiovascular activity. At the same time, tsepsis was induced by cecal ligation and puncture (CLP). The FAAH inhibitor URB597, in the dose of 0,6mgl/kg, was injected intravenous immediately after the end of the surgery, and the cardiovascular parameters were measured during a period of 8h. Institution’s Animal Ethics Committee (N -082/2010). The intravenous treatment with URB597, a FAAH inhibitor, did not affect the basal BP (PAM = 97±4 vs 96±3 mmHg; t= 0.6, p>0.05 n=5) and HR, and HR (343±4 vs 345±4 bpm; t=0.2; p>0.05). However, the treatment with URB597 increased the fall in the BP (F(1,294)= 17, p<0.0001) and decreased the characteristic tachycardia (F(1,294)=54, p<0,0001) observed during the septic shock caused by CLP. The present results indicate that endocannabinoids participate in the genesis of the cardiovascular changes observed during septic shock caused by CLP.