Abstract
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 DesArg(9)BK (DBK). Our aim was to determine the potential expression of kinin B(1) and B(2) 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 (pD(2)) 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 microM norepinephrine. The concentration-dependent responses of BK and DBK were markedly inhibited by the arachidonic acid inhibitor indomethacin (1 microM), 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 B(1) and B(2) subtypes of kinin receptors and that stimulation with BK and DBK induces contractile effect mediated by endothelium-independent vasoconstrictor prostanoids.
Highlights
Kinins are proinflammatory peptides that act as local hormones and activate the release of endothelium-derived relaxing factors such as nitric oxide (NO) and prostaglandins, increase vascular permeability, relax or contract smooth muscle, and provoke pain
Bradykinin (BK)- and DesArg9BK (DBK)-induced isometric contractile responses were assessed in the absence and in the presence of 1 μM indomethacin, a cyclooxygenase inhibitor, preincubated for 20 min
We assessed the role of B1 and B2 receptors in mouse abdominal aorta using isometric force measurements
Summary
Kinins are proinflammatory peptides that act as local hormones and activate the release of endothelium-derived relaxing factors such as nitric oxide (NO) and prostaglandins, increase vascular permeability, relax or contract smooth muscle, and provoke pain (for a review, see Ref. 1). Most of these effects of kinins are mediated by the activation of the B2 receptor, which belongs to a family of peptide hormone receptors linked to G proteins, via the agonist bradykinin (BK). In this study we demonstrate that BK and DBK did not relax but induced endothelium-independent contractions of mouse abdominal aorta in a concentration-dependent fashion. These contractile responses to the kinins in rings of abdominal aorta were associated with the production of eicosanoids, whereas NO involvement was not demonstrable
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callMore From: Brazilian Journal of Medical and Biological Research
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
