Induction of kinin B₁ receptor‐dependent vasoconstriction following balloon catheter injury to the rabbit carotid artery

Abstract

Balloon catheter injury to the rabbit carotid artery damaged the endothelium and induced neointima formation over 7 days. The area of intima, expressed as a percentage of the media, was 16.2 ± 4.2% and 8.2 ± 0.1% in balloon catheter‐injured and sham‐operated arteries. Seven days after arterial injury, carotid arteries were isolated and set up as ring preparations in organ baths for isometric tension measurements. Balloon catheter‐injured arteries first contracted with noradrenaline (0.01–0.1 μ m ), contracted further in a concentration‐dependent manner to bradykinin (BK; pD 2 , 5.98 ± 0.22; E max , 41.3 ± 5.2% of KCl) and to des‐Arg 9 ‐BK (pD 2 , 7.12 ± 0.36; E max , 46.0 ± 9.9% of KCl). In contrast, vessel segments with endothelium either intact or acutely removed were unresponsive to both BK receptor agonists. The concentration‐contraction curves for BK and for des‐Arg 9 ‐BK were shifted to the right by the B 1 receptor antagonist, [Leu 8 ]des‐Arg 9 ‐BK (3 μ m ), but not by the selective B 2 receptor antagonist, Hoe 140 (1 μ m ). Thus, BK and its metabolite, des‐Arg 9 ‐BK act as vasoconstrictor agents following balloon catheter injury. These effects appear to be mediated by activation of B 1 receptors.