Introduction: Angiogenesis depends on a complex network of cells and mediators. The activation or blockade of annabinoid receptors showed to be an interesting pharmacological strategy to attenuate the angiogenic and/or inflammatory response in many experimental models. Here we investigated how this strategy may interfere in inflammatory angiogenesis. Methods: Polyester-polyurethane sponges were implanted in C57BL/6 mice. Animals received daily doses (10 mg/kg, s.c.) of the cannabinoid antagonists SR141716A (CB1) and SR144528 (CB2), separately, or 3 mg/Kg (s.c.) of the cannabinoid CB1/CB2 agonist WIN 55212-2, for 7 or 14 days. The implants were then collected for ELISA, hemoglobin, myeloperoxidase and N-acetylglucosaminidase measurements, used as indexes for angiogenesis, neutrophil and macrophage accumulation, respectively. Results: CB1 or CB2 receptor antagonist treatment was able to reduce cellular influx to the sponge at 7 and 14 days, with distinctive pattern for macrophages and neutrophils. The CB1/CB2 agonist also reduced cellular influx. Both treatments affected angiogenesis. These alterations were accompanied by changes in the levels of TNF-a, VEGF, CXCL1-3/KC, CCL2/JE and RANTES in all treatments. Discussion: The blockade or activation of cannabinoid receptors showed to be effective in reducing inflammatory and angiogenic responses. Altough acting in a similar way, different levels of cytokines and chemokines may help explain this paradoxal response.