Wahl M, Young A R, Edvinsson L, Wagner F
J Cereb Blood Flow Metab. 1983 Jun;3(2):231-7. doi: 10.1038/jcbfm.1983.31.
The effect of bradykinin on cerebrovascular resistance vessels was investigated by the use of in vitro and in situ preparations. Bradykinin, in the range of 10(-10) to 10(-5) M, elicited a concentration-dependent vasodilatation on both feline and human pial arteries in vitro; the half-maximal response was found to be approximately at 2.8 X 10(-7) M and 1.3 X 10(-8) M (EC50), respectively. This dilatatory effect of bradykinin in vitro was found only in arteries preconstricted with prostaglandin F2 alpha or 5-hydroxytryptamine. In order to determine the effects of bradykinin on the diameter of cat pial arteries in situ, perivascular microapplication was employed. The dose-response curves obtained showed vasodilatation; the EC50 and the maximal response (EAm) were 4.4 X 10(-7) M and 45.5% at 10(-5) M, respectively. Statistically significant (p less than 0.01) reactions were observed at 10(-7) M and higher concentrations of bradykinin. The observed effects were independent of initial vessel size (80-260 microns). These in situ findings are very similar to those found in vitro. The isolated guinea pig ileum was used to check the stability of the bradykinin solutions. In this instance, a concentration-dependent contraction was found when "freshly prepared" or "5 hours stored" bradykinin was applied, indicating no measureable degradation of bradykinin. We conclude that bradykinin is a powerful vasodilator of both human and feline pial arteries.
通过体外和原位制备方法研究了缓激肽对脑血管阻力血管的作用。在10^(-10)至10^(-5)M范围内,缓激肽在体外对猫和人的软脑膜动脉均引起浓度依赖性血管舒张;半最大反应分别约为2.8×10^(-7)M和1.3×10^(-8)M(EC50)。缓激肽在体外的这种舒张作用仅在预先用前列腺素F2α或5-羟色胺收缩的动脉中发现。为了确定缓激肽对猫软脑膜动脉原位直径的影响,采用了血管周围微量给药法。得到的剂量反应曲线显示血管舒张;EC50和最大反应(EAm)分别为4.4×10^(-7)M和10^(-5)M时的45.5%。在10^(-7)M及更高浓度的缓激肽下观察到具有统计学意义(p<0.01)的反应。观察到的效应与初始血管大小(80 - 260微米)无关。这些原位研究结果与体外研究结果非常相似。使用分离的豚鼠回肠检查缓激肽溶液的稳定性。在这种情况下,当应用“新鲜制备”或“储存5小时”的缓激肽时,发现浓度依赖性收缩,表明缓激肽没有可测量的降解。我们得出结论,缓激肽是人和猫软脑膜动脉的强效血管舒张剂。