INDUCTION OF KININ B-1 RECEPTOR-DEPENDENT VASOCONSTRICTION FOLLOWING BALLOON CATHETER INJURY TO THE RABBIT CAROTID-ARTERY

1 Balloon catheter injury to the rabbit carotid artery damaged the end othelium and induced neointima formation over 7 days. The area of inti ma, 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. 2 Sev en days after arterial injury, carotid arteries were isolated and set up as ring preparations in organ baths for isometric tension measureme nts. Balloon catheter-injured arteries first contracted with noradrena line (0.01-0.1 muM), contracted further in a concentration-dependent m anner to bradykinin (BK; pD2, 5.98 +/- 0.22; E(max), 41.3 +/- 5.2% of KCl) and to des-Arg9-BK (pD2, 7.12 +/- 0.36; E(max), 46.0 +/- 9.9% of KCl). In contrast, vessel segments with endothelium either intact or a cutely removed were unresponsive to both BK receptor agonists. 3 The c oncentration-contraction curves for BK and for des-Arg9-BK were shifte d to the right by the B1 receptor antagonist, [Leu8]des-Arg9-BK (3 muM ), but not by the selective B2 receptor antagonist, Hoe 140 (1 muM). 4 Thus, BK and its metabolite, des-Arg9-BK act as vasoconstrictor agent s following balloon catheter injury. These effects appear to be mediat ed by activation of B1 receptors.