Disruption of the kinin B1 receptor gene affects potentiating effect of captopril on BK-induced contraction in mice stomach fundus

A transgenic mouse model, deficient in kinin B1 receptor (B1−/−) was used to evaluate the role of B2 receptor in the smooth muscle stomach fundus. The results showed that the potency of bradykinin (BK) to induce contraction in the gastric tissue was maintained whereas the efficacy was markedly reduced. The angiotensin converting enzyme (ACE) inhibitor captopril potentiated BK-induced effect in wild type (WT) but not in B1−/− fundus. However, ACE activity detected by the convertion of Ang I to Ang II was inhibited by captopril in both types of gastric tissues. Taking into account the hypothesis that captopril and ACE bind to the B2 receptor, we suggest that this complex was not formed in the stomach deficient in B1 receptor. Therefore, our finding strongly support the hypothesis that in smooth muscles that constitutively express the kinin B1 and B2 receptors, an interaction between captopril and ACE, B1 and B2 receptors should occur forming a complex protein interaction for the potentiating effect of ACE on kinin receptors.