ABSTRACT
The aim of this study was to evaluate the effect of angiotensin II on models of acute inflammation. This study shows that angiotensin II potentiates the carrageenan- and dextran-induced paw edema. The administration of angiotensin II does not change the myeloperoxidase activity, neither the tissue content of interleukin-1 beta and tumor necrosis alpha nor the neutrophil migration to the peritoneal cavity, but induces significant enhancement of mast cell degranulation. The anti-histamine, mepyramine, and the anti-serotonin, metisergyde, reduce the angiotensin II-facilitated dextran-induced edema. Our results suggest that angiotensin II increases the vascular permeability through induction of mast cell degranulation and that this effect is mediated by the angiotensin AT2 receptor, since the angiotensin AT1 receptor antagonist and the angiotensin AT2 receptor agonist potentiated the paw edema.
