Change in the microcirculatory hemodynamic is one of the most important event in the inflammation. In the dental pulp, which is a connective tissue surrounded by a mineralized dentine, the disturb in the blood flow and plasma extravasatioin can lead to the increase of pulp pressure and ischemia. Vasoactive peptides play an active role in homeostatic regulation of the pulp physiology by controlling the blood flow as well as regulating the inflammation and healing process. The octapeptide angiotensin II (AngII) regulates vascular tone and stimulates the release of pro-inflammatory cytokines by acting through the AT₁ and AT₂ receptors. The AT₁ receptor is responsible for the classical effects of AngII. The AT₂ receptor is expressed at high level in fetal tissues and some of its effects, such as vasodilatation, are opposite to those of the AT₁ receptor. The aim of this study was to evaluate the role of AT₁ and AT₂ receptors on the pulpal inflammation. Class I cavities were drilled on the oclusal surface of first molars of Wistar rats. The pulp tissue was mechanically exposed. After 3, 6, 9, 12 and 24-hour periods the teeth were extracted and submitted to the histopathological and RT-PCR analyses. Non-exposed teeth were used as controls. The histological sections stained with H/E showed a number of congested and dilated blood vessels associated with a notable presence of inflammatory cells. RT-PCR data revealed that the AT₁ receptor was sistematically down-regulated up to 24 hours of pulp exposure. However, the AT₂ receptor was up-regulated until 9-hour period and then slightly down-regulated. It was demonstrated that the renin-angiotensin system play an important role in the pulpal inflammation, probably by an opposite regulation of AngII receptors level. Financial Support: FAPESP, CNPq, FAEPA.