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在36只隔离灌流颈动脉窦区的麻醉大鼠上,观察了八肽胆囊收缩素(cholecystokinin octapeptide,CCK-8)对颈动脉窦压力感受器反射的影响。其结果如下:(1)以CCK-8(0.1、0.5、1.0 μmol/L)隔离灌流颈动脉窦区时,压力感受器机能曲线向右上方移位,曲线最大斜率(peak slope,PS)减小,反射性血压下降幅度(reflex decrease,RD)减少,阈压(thresholdpressure,TP)和饱和压(saturation pressure,SP)均增高。其中RD、PS和TP呈明显的剂量依赖性;(2)用CCK-8的非特异性受体拮抗剂丙谷胺(100μmol/L)预处理后,能明显减弱CCK-8(0.5μmol/L)对压力感受器反射的抑制;(3)预先灌流一氧化氮合酶(nitric oxide synthase.NOS)阻断剂(L-NAME,100 μmol/L),不能阻断CCK-8(0.5 μmol/L)对压力感受器反射的影响:(4)用Ca2+通道激动剂Bay K 8644(500 nmol/L)预处理后,也能明显减弱CCK-8(0.5 μmol/L)对压力感受器反射的抑制作用。以上结果提示,CCK-8是通过作用于颈动脉窦压力感受器神经元末梢上的受体而起到抑制作用的,其机制可能为抑制了牵张敏感性通道,致使Ca2+离子内流减少,而与内皮细胞释放NO无关。
The effects of cholecystokinin octapeptide (CCK-8) on carotid sinus baroreceptor reflex were observed in 36 anesthetized rats with isolated perfused carotid sinus. The results were as follows: (1) When perfusing the carotid sinusoids with CCK-8 (0.1, 0.5 and 1.0 μmol / L), the baroreceptor function curve shifted to the upper right and the peak slope (PS) , Decreased reflex decrease (RD), increased threshold pressure (TP) and saturation pressure (SP). (2) CCK-8 (0.5μmol / L) pretreated with 100μmol / L CCK-8, a nonspecific receptor antagonist, ) Inhibited the baroreflex reflex. (3) Pretreatment of nitric oxide synthase (NOS) blocker (100 μmol / L) blocked CCK-8 (0.5 μmol / L ) On baroreflex reflectance: (4) Inhibition of baroreflex reflex by CCK-8 (0.5 μmol / L) was also significantly attenuated by pretreatment with Ca2 + channel agonist Bay K 8644 (500 nmol / L) The above results suggest that CCK-8 plays an inhibitory role by acting on the receptors of the neurons of the carotid sinus baroreceptor, and its mechanism may be to inhibit the stretch-sensitive channels and reduce the influx of Ca 2+ ions Nothing to do with the release of NO from endothelial cells.