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

C. Mazenot, L. Loufrani*, D. Henrion*, C. Ribuot, W. Müller-Esterl† and D. Godin-Ribuot

1. Kinin B₁-receptors are induced by various inflammatory stimuli. Since myocardial ischaemia-reperfusion results in inflammation, we questioned whether it could induce B₁-receptor-dependent responses to des-Arg⁹-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 g kg^-1, intra-arterial: -12 ± 2 vs. -5 ± 2 mmHg in the sham group, P < 0.02), which was significantly antagonised by [Leu⁸]-des-Arg⁹-bradykinin (LBK), a B₁-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 B₁-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 B1-receptors in the endothelium.

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