Actions of bradykinin and related peptides on rabbit coeliac artery rings

Abstract

Rabbit coeliac artery rings were mounted in tissue baths containing Krebs solution at 37°C in order to determine whether their response to bradykinin is initiated by B1 or B2‐receptors. Tension was recorded isometrically. Phenylephrine contracted the tissue. Subsequent addition of bradykinin or des Arg10‐kallidin caused relaxation which was not dependent on an intact endothelium. Des Arg10‐kallidin, a B1‐receptor selective agonist, was more potent than bradykinin. [β‐Thienyl alanyl6,9, D‐Phe8]‐kallidin and [Leu9]‐des Arg10‐kallidin antagonized bradykinin and des Arg10‐kallidin. [Leu9]‐des Arg10‐kallidin, a B1‐receptor selective antagonist, was more potent than [Thi69, D‐Phe8]‐kallidin, a less selective drug that acts on both B1 and B2‐receptors. Kinin‐induced relaxation was reversibly antagonized by ibuprofen (a cyclo‐oxygenase inhibitor) and by 5‐(N,N‐hexamethylene)amiloride (an inhibitor of Na+/H+ exchange). Ibuprofen caused a parallel shift to the right of a semi‐logarithmic plot of the agonist concentration‐effect relationship, whereas the amiloride analogue depressed the maximum response and reduced the slope. We conclude that bradykinin and des Arg10‐kallidin relax rabbit coeliac artery by combining with B1‐receptors. The response is mediated by a cyclo‐oxygenase product and may be influenced by cellular Na+/H+ exchange. 1989 British Pharmacological Society