Elucidation of vasoreactive diversity induced by bradykinin -studies of G-proteins function and bradykinin metabolism -

（1）培养的猪基底动脉内皮细胞在无刺激条件下可自发释放一氧化氮（NO）。缓激肽（BK）以浓度依赖性方式促进NO的产生。选择性B_2受体拮抗剂HOE 140或NO合成酶抑制剂L-硝基精氨酸可抑制NO的产生。（2）血管紧张素（Ang）Ⅱ可引起离体猪基底动脉环收缩。选择性B_2受体拮抗剂HOE 140可抑制Ang Ⅱ引起的收缩，而血管紧张素转换酶（ACE）抑制剂卡托普利则增强Ang Ⅱ引起的收缩。(3)BK在离体猪基底动脉环中诱导内皮依赖性舒张，随后是收缩。在L-硝基精氨酸（10 μ M）存在下<-4>，BK引起收缩但不舒张。血管紧张素Ⅱ（Ang）受体拮抗剂氯沙坦（Losartan）不抑制BK引起的收缩，提示缓激肽与Ang受体之间可能存在相互作用。在这一点上似乎需要进一步的实验。

(1)Nitric oxide (NO) is spontaneously released from cultured porcine basilar arterial endothelial cells under no stimulation conditions. Bradykinin (BK) enhanced the NO production in a concentration-dependent manner. The enhanced NO production was inhibited by treatments of a selective B_2 receptor antagonist, HOE140, or a NO synthase inhibitor, L-nitro-arginine.(2)Angiotensin (Ang) II induced a contraction in isolated porcine basilar arterial ring. A selective B_2 antagonist, HOE140, inhibited the AngII-induced contraction, while an Ang converting enzyme (ACE) inhibitor, captopril, enhanced the Ang II-induced contraction.(3)BK induces endothelium-dependent relaxation following by contraction in isolated porcine basilar arterial ring. In the presence of L-nitro-arginine (10^<-4> M), BK induced contraction but not relaxation. The BK-induced contraction was not inhibited by a selective AT_1 receptor antagonist, losartan.These results suggest that there might be some interaction between bradykinin and Ang receptors. Further experiments appears to be needed in this point.