生理学报
生理學報
생이학보
ACTA PHYSIOLOGICA SINICA
2004年
1期
25-30
,共6页
刘宜先%张浩%马会杰%何瑞荣
劉宜先%張浩%馬會傑%何瑞榮
류의선%장호%마회걸%하서영
八肽胆囊收缩素%丙谷胺%Bay K 8644%压力感受器反射%L-NAME%平均动脉压
八肽膽囊收縮素%丙穀胺%Bay K 8644%壓力感受器反射%L-NAME%平均動脈壓
팔태담낭수축소%병곡알%Bay K 8644%압력감수기반사%L-NAME%평균동맥압
cholecystokinin octapeptide (CCK-8)%proglumide%Bay K 8644%baroreflex%L-NAME%mean arterial pressure
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(100 μmol/L)预处理后,能明显减弱CCK-8(0.5 μmol/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(05μmol/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(0.5μmol/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.
在36隻隔離灌流頸動脈竇區的痳醉大鼠上,觀察瞭八肽膽囊收縮素(cholecystokinin octapeptide,CCK-8)對頸動脈竇壓力感受器反射的影響.其結果如下:(1)以CCK-8(0.1、0.5、1 0 μmol/L)隔離灌流頸動脈竇區時,壓力感受器機能麯線嚮右上方移位,麯線最大斜率(peak slope,PS)減小,反射性血壓下降幅度(reflex decrease,RD)減少,閾壓(thresholdpressure,TP)和飽和壓(saturation pressure,SP)均增高.其中RD、PS和TP呈明顯的劑量依賴性;(2)用CCK-8的非特異性受體拮抗劑丙穀胺(100 μmol/L)預處理後,能明顯減弱CCK-8(0.5 μmol/L)對壓力感受器反射的抑製;(3)預先灌流一氧化氮閤酶(nitric oxide synthase,NOS)阻斷劑(L-NAME,100 μmol/L),不能阻斷CCK-8(05μmol/L)對壓力感受器反射的影響;(4)用Ca2+通道激動劑Bay K 8644(500 nmol/L)預處理後,也能明顯減弱CCK-8(0.5μmol/L)對壓力感受器反射的抑製作用.以上結果提示,CCK-8是通過作用于頸動脈竇壓力感受器神經元末梢上的受體而起到抑製作用的,其機製可能為抑製瞭牽張敏感性通道,緻使Ca2+離子內流減少,而與內皮細胞釋放NO無關.
재36지격리관류경동맥두구적마취대서상,관찰료팔태담낭수축소(cholecystokinin octapeptide,CCK-8)대경동맥두압력감수기반사적영향.기결과여하:(1)이CCK-8(0.1、0.5、1 0 μmol/L)격리관류경동맥두구시,압력감수기궤능곡선향우상방이위,곡선최대사솔(peak slope,PS)감소,반사성혈압하강폭도(reflex decrease,RD)감소,역압(thresholdpressure,TP)화포화압(saturation pressure,SP)균증고.기중RD、PS화TP정명현적제량의뢰성;(2)용CCK-8적비특이성수체길항제병곡알(100 μmol/L)예처리후,능명현감약CCK-8(0.5 μmol/L)대압력감수기반사적억제;(3)예선관류일양화담합매(nitric oxide synthase,NOS)조단제(L-NAME,100 μmol/L),불능조단CCK-8(05μmol/L)대압력감수기반사적영향;(4)용Ca2+통도격동제Bay K 8644(500 nmol/L)예처리후,야능명현감약CCK-8(0.5μmol/L)대압력감수기반사적억제작용.이상결과제시,CCK-8시통과작용우경동맥두압력감수기신경원말소상적수체이기도억제작용적,기궤제가능위억제료견장민감성통도,치사Ca2+리자내류감소,이여내피세포석방NO무관.
The purpose of this study was to determine the effect of cholecystokinin octapeptide (CCK-8) on carotid sinus baroreflex in 36 anesthetized male rats by isolated carotid sinus perfusion in vivo. The results obtained are as follows. (1) By perfusion with CCK-8 (0.1, 0.5, 1.0 μmol/L), the functional curve of baroreflex was shifted to the right and upward, with a decrease in peak slope (PS) (P＜0.001) and a reflex decrease (RD) in mean arterial pressure, while the threshold pressure (TP) and saturation pressure (SP) were significantly increased. Among the functional parameters of carotid sinus baroreflex, the changes in RD, PS and TP were dose-dependent. (2) Pretreatment with proglumide (100 μmol/L), a nonselective CCK receptor antagonist,the inhibitory effect of CCK-8 (0.5 μmol/L) on the baroreflex was significantly attenuated. (3) Pretreatment with L-NAME (100μmol/L), an inhibitor of nitric oxide (NO) synthase, did not affect the inhibitory action of CCK-8 (0.5 μmol/L). (4) Preperfusion with Bay K 8644 (500 nmol/L), an agonist of calcium channel, could attenuate the effect of CCK-8 (0.5 μmol/L). It is suggested that the inhibitory action of CCK-8 on the baroreflex may be mediated by the activation of its receptors in the carotid sinus baroreceptor, leading to an inhibition of stretch-sensitive channels and a decrease in Ca2+ influx. However, NO released from the endothelium seems not to be involved in the mechanism of this effect.
