Görlach C, Wahl M
Department of Physiology, LMU Munich, Germany.
Peptides. 1996;17(8):1373-8. doi: 10.1016/s0196-9781(96)00223-9.
Ring segments of rat middle cerebral artery (MCA) were prepared for measurement of isometric force and precontracted with 10(-4) M uridine triphosphate (UTP). Concentration-effect curves (CEC) were constructed for bradykinin (BK, 10(-8)(-10)(-1) M) in segments with functionally intact (E+) or denuded (E-) endothelium. E- segments did not dilate to BK. The BK receptor was characterized by application of specific B1 or B2 antagonists [des-Arg4-Leu8] BK (10(-5) M) and [D-Arg4-Hyp3-Thi5-D-Tic7-Oic8] BK (HOE140, 3 x 10(-7) M), respectively, or B2 agonist [des-Arg9] BK (10(-8)-10(-4) M). Involvement of nitric oxide (NO) was tested with NG-nitro-L-arginine (LNNA, 10(-4) M). BK induced concentration-dependent relaxation with a maximal effect (Emax) of 40.86 +/- 1.50% at 10(-4) M and a pD2 (-log10 EC50) of 6.818 +/- 0.044. This relaxation could be prevented with HOE140 or LNNA, but was not influenced by [des-Arg(9)-Leu] BK. [des-Arg9] BK did not induce any effect. These results demonstrate that BK induced relaxation via endothelial B2 receptors and release of NO in isolated rat MCA.
制备大鼠大脑中动脉（MCA）的血管环用于等长力测量，并先用10⁻⁴ M三磷酸尿苷（UTP）进行预收缩。构建了缓激肽（BK，10⁻⁸ - 10⁻¹ M）在具有功能完整（E⁺）或去内皮（E⁻）的血管环中的浓度 - 效应曲线（CEC）。E⁻血管环对BK不产生舒张反应。通过分别应用特异性B1或B2拮抗剂[去 - Arg⁴ - Leu⁸] BK（10⁻⁵ M）和[D - Arg⁴ - Hyp³ - Thi⁵ - D - Tic⁷ - Oic⁸] BK（HOE140，3×10⁻⁷ M）或B2激动剂[去 - Arg⁹] BK（10⁻⁸ - 10⁻⁴ M）来对BK受体进行表征。用NG - 硝基 - L - 精氨酸（LNNA，10⁻⁴ M）检测一氧化氮（NO）的参与情况。BK诱导浓度依赖性舒张，在10⁻⁴ M时最大效应（Emax）为40.86±1.50%，pD2（-log₁₀ EC₅₀）为6.818±0.044。这种舒张可被HOE140或LNNA阻断，但不受[去 - Arg(9) - Leu] BK影响。[去 - Arg⁹] BK未诱导任何效应。这些结果表明，在离体大鼠MCA中，BK通过内皮B2受体诱导舒张并释放NO。
