Resumo

Introduction: Kinin, a class of polypeptides represented by bradykinin, kallidin, and their metabolites, acting via B1 and B2 receptors, have been related to cytokines action, glutamate release and prostaglandin production. Several studies indicate that in the central nervous system and peripheral tissues, estrogen regulates the expression of B2 receptor and reduces inflammatory response. Accordingly, the present work aimed to investigate expression of kinin B2 receptors in female rats submitted to the pilocarpine model of epilepsy. Methods: The animals were divided in four groups: OVX + SE ovariectomized female rats, which presented status epilepticus (SE); SE: intact female rats that presented SE; OVX ovariectomized female rats that received saline instead of pilocarpine; SAL intact female rats that received saline instead pilocarpine. The hippocampi from all groups were removed 5h (acute group), 5 days (silent group) and 60 days (chronic group). The hippocampi from all groups were used to perform the distribution and quantification of kinin B2 receptor by Western Blotting (n=4 per group) and immuno-histochemistry (n=3 per group). Results: the results showed a decrease of immunoreactivity of kinin B2 receptor in the hippocampal formation during the acute and silent but not in chronic periods of this model in SE group when compared to SAL group. In contrast, the immunoreactivity in OVX + SE group was increased during the acute and silent periods when compared with OVX group. The Western Blotting showed an increased expression of kinin B2 receptor in OVX +SE group during the acute (2872.42„b236.82) (p=0.0034) and silent periods (2391.32„b188.18) (p=0.0277), when compared with its proper controls (OVX) (1739.08„b425.16). In addition, a decreased expression in SE group during the acute (1171.35„b259.73) (p=0.0039) and silent periods (1661.87„b345.55, p=0.0121) were found, when compared with controls (SAL, 2470.92„b509.58). Conclusions: This study showed that the expression of kinin B2 receptor is modified in female rats during epileptogenesis and modulated by steroid hormones.