Artículos de revistas
Functional expression of kinin B1 and B2 receptors in mouse abdominal aorta
Fecha
2007-05-01Registro en:
Brazilian Journal of Medical and Biological Research. Associação Brasileira de Divulgação Científica, v. 40, n. 5, p. 649-655, 2007.
0100-879X
S0100-879X2007000500007.pdf
S0100-879X2007000500007
10.1590/S0100-879X2006005000087
WOS:000246576900007
Autor
Felipe, Sandra Arantes
Rodrigues, Eliete da Silva
Martin, Renan Paulo
Paiva, Antonio Cechelli de Mattos
Pesquero, João Bosco
Shimuta, Suma Imura
Institución
Resumen
Previous studies have shown that the vascular reactivity of the mouse aorta differs substantially from that of the rat aorta in response to several agonists such as angiotensin II, endothelin-1 and isoproterenol. However, no information is available about the agonists bradykinin (BK) and DesArg9BK (DBK). Our aim was to determine the potential expression of kinin B1 and B2 receptors in the abdominal mouse aorta isolated from C57BL/6 mice. Contraction and relaxation responses to BK and DBK were investigated using isometric recordings. The kinins were unable to induce relaxation but concentration-contraction response curves were obtained by applying increasing concentrations of the agonists BK and DBK. These effects were blocked by the antagonists Icatibant and R-715, respectively. The potency (pD2) calculated from the curves was 7.0 ± 0.1 for BK and 7.3 ± 0.2 for DBK. The efficacy was 51 ± 2% for BK and 30 ± 1% for DBK when compared to 1 µM norepinephrine. The concentration-dependent responses of BK and DBK were markedly inhibited by the arachidonic acid inhibitor indomethacin (1 µM), suggesting a mediation by the cyclooxygenase pathway. These contractile responses were not potentiated in the presence of the NOS inhibitor L-NAME (1 mM) or endothelium-denuded aorta, indicating that the NO pathway is not involved. We conclude that the mouse aorta constitutively contains B1 and B2 subtypes of kinin receptors and that stimulation with BK and DBK induces contractile effect mediated by endothelium-independent vasoconstrictor prostanoids.