| Institution: | 1.Departamento de Fisiologia,Universidade Federal de Santa Catarina,Brazil;2.Departamento de Biologia Celular, Embriologia e Genética,Universidade Federal de Santa Catarina,Brazil;3.Departamento de Neurologia, Psiquiatria e Psicologia Médica,Faculdade de Medicina de Ribeir?o Preto, Universidade de S?o Paulo,S?o Paulo,Brazil;4.Departamento de Cirurgia, Faculdade de Medicina de Ribeir?o Preto,Universidade de S?o Paulo,S?o Paulo,Brazil;5.Centro de Cirurgia de Epilepsia,Hospital Governador Celso Ramos,Florianópolis,Brazil;6.Centro de Ciências da Saúde,Faculdade de Medicina da Universidade do Vale do Itajaí, UNIVALI,Itajaí,Brazil |
| Abstract: | BackgroundWhile it is well known that bradykinin B2 agonists increase plasma protein extravasation (PPE) in brain tumors, the bradykinin B1 agonists tested thus far are unable to produce this effect. Here we examine the effect of the selective B1 agonist bradykinin (BK) Sar-D-Phe8]des-Arg9BK (SAR), a compound resistant to enzymatic degradation with prolonged activity on PPE in the blood circulation in the C6 rat glioma model.ResultsSAR administration significantly enhanced PPE in C6 rat brain glioma compared to saline or BK (p < 0.01). Pre-administration of the bradykinin B1 antagonist Leu8]-des-Arg (100 nmol/Kg) blocked the SAR-induced PPE in the tumor area.ConclusionsOur data suggest that the B1 receptor modulates PPE in the blood tumor barrier of C6 glioma. A possible role for the use of SAR in the chemotherapy of gliomas deserves further study. |
