Interaction of bradykinin and des-Arg9-bradykinin with isolated pig coronary arteries: mechanical and electrophysiological events.

This paper describes the effect of bradykinin (BK) and des-Arg9-BK on the isometric tension and smooth muscle membrane potential of transverse strips of pig coronary artery. BK causes a relaxation of contracted muscle. This effect is particularly evident in muscle which has previously been contracted by acetylcholine. The relaxation is accompanied by a transient hyperpolarization of the vascular smooth muscle. Des-Arg9-BK, in contrast, causes a contraction of the muscle which is not accompanied by a significant change of transmembrane potential. The relaxing action of BK depends on the presence of the endothelium. In a "cascade" experiment, evidence is presented that a relaxing factor is released by the endothelium in response to BK. Thus the perfusate from a BK-stimulated intact artery can cause the relaxation of a pre-contracted de-endothelialized artery. We conclude that the endothelium has B2-receptors which cause the release of a humoral factor which hyperpolarizes and relaxes the muscle. The contracting action of des-Arg9-BK does not depend on the endothelium and appears to be mediated through B1-receptors directly on smooth muscle by pharmacomechanical coupling.