The present study was undertaken to demonstrate the presence of bradykinin B1 receptors mediating contraction of human umbilical vein. The bradykinin B1 receptor selective agonist, des-Arg9-bradykinin, produced a dose-dependent contractile response of human umbilical vein rings. Furthermore, des-Arga-bradykinin-mediated response increased in a time-dependent manner in vitro. The maximal response to des-Arg9-bradykinin, expressed as percentage of the maximum elicited by serotonin, was: 10 +/- 2 at 15 min, 55 +/- 5 at 120 min and 80 +/- 3 at 300 min. Des-Arg9-bradykinin-mediated contractions were inhibited by the specific bradykinin B1 receptor antagonist des-Arg9-[Leu8]bradykinin which produced parallel shifts in the dose-response curve to the selective bradykinin B1 receptor agonist. Schild regression analysis of data established a pA2 value of 6.16 +/- 0.06. Kinin-induced contraction was not modified by pre-treatment with indomethacin (10 microM), a cyclo-oxygenase inhibitor. On the other hand, continuous exposure to the anti-inflammatory steroid dexamethasone (100 microM) or to the protein synthesis inhibitor cycloheximide (70 microM) largely prevented the sensitization to des-Arg9-bradykinin in incubated human umbilical vein rings. These results confirm the presence of bradykinin B1 receptors which mediate contraction in isolated human umbilical vein. These responses are up-regulated in a time- and protein synthesis-dependent process.