Actions of bradykinin and related peptides on rabbit coeliac artery rings

1 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. 2 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. 3 [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. 4 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. 5 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.