Endothelial kinin B1-receptors are induced by myocardial ischaemia-reperfusion in the rabbit

1. Kinin B-1-receptors are induced by various inflammatory stimuli. Since myocardial ischaemia-reperfusion results in inflammation, we questioned whether it could induce B-1-recepbor-dependent responses to des-Arg(9)-bradykinin (DBK). 2. Thirty-six rabbits were submitted either to a 30 min coronary occlusion followed by a 3 h reperfusion or to a sham operation. The response to DBK was then tested in vivo on mean arterial pressure (MAP) and in vitro on isolated hearts and arterial rings. 3. DBK induced a dose-dependent decrease in MAP in the ischaemia-reperfusion group (DBK, 10 mug kg(-1), intra-arterial: -12 +/- 2 vs. -5 +/- 2 mmHg in the sham group, P < 0.02), which was significantly antagonised by [Leu(8)]-des-Arg(9)-bradykinin (LBK), a B-1-receptor antagonist. Following ischaemia-reperfusion, isolated hearts responded to DBK by a decrease in coronary perfusion pressure greater than that of the sham group. DBK dose-dependently decreased the isometric force of isolated carotid rings (DBK, 10(-5) M: -9 +/- 2 vs. -1 +/- 2 % in the sham group, P < 0.02) and mesenteric arteries (DBK, 10(-6) M: -38 +/- 7 % vs. -3 +/- 2 % in the sham group, P < 0.001). The vascular effects of DBK seen after ischaemia-reperfusion were significantly antagonised by LBK. The presence of B-1-receptors in ischaemia-reperfusion animals was confirmed by immunolocalisation and Western blot analysis. 4. This study demonstrates that myocardial ischaemia-reperfusion induces a global induction of functional kinin B-1-receptors in the endothelium.