中国药理学与毒理学杂志
中國藥理學與毒理學雜誌
중국약이학여독이학잡지
CHINESE JOURNAL OF PHARMACOLOGY AND TOXICOLOGY
2005年
1期
18-23
,共6页
刘宜先%张浩%董京辉%李茜%何瑞荣
劉宜先%張浩%董京輝%李茜%何瑞榮
류의선%장호%동경휘%리천%하서영
八肽胆囊收缩素%颈动脉窦%压力感受器%丙谷胺%Bay K8644%NG-硝基-L-精氨酸甲酯
八肽膽囊收縮素%頸動脈竇%壓力感受器%丙穀胺%Bay K8644%NG-硝基-L-精氨痠甲酯
팔태담낭수축소%경동맥두%압력감수기%병곡알%Bay K8644%NG-초기-L-정안산갑지
cholecystokinin octapeptide%carotid sinus%pressoreceptors%proglumide%Bay K8644%NG-nitro-L-arginine methylester
目的观察八肽胆囊收缩素(CCK-8)是否通过直接抑制颈动脉窦压力感受器放电活动而影响心血管功能.方法在麻醉雄性大鼠隔离灌流颈动脉窦区条件下记录窦神经传入放电及积分.结果① CCK-8 0.1,0.5和1.0 μmol·L-1使压力感受器机能曲线向右下方移位,曲线最大斜率和窦神经传入放电积分最大值均明显减小,表明CCK-8可剂量依赖性抑制颈动脉窦压力感受器活动.②预先灌流CCK-8非特异性受体阻断剂丙谷胺100 μmol·L-1或钙通道开放剂Bay K8644 0.5 μmol·L-1可部分阻断CCK-8 0.5 μmol·L-1对颈动脉窦压力感受器放电活动的抑制作用.预先灌流一氧化氮合酶抑制剂L-NAME不能阻断CCK-8的效应.结论 CCK-8可直接抑制大鼠颈动脉窦压力感受器传入神经放电活动.其机制可能为CCK-8作用于颈动脉窦区相应的受体后,对牵张敏感性通道产生抑制作用.
目的觀察八肽膽囊收縮素(CCK-8)是否通過直接抑製頸動脈竇壓力感受器放電活動而影響心血管功能.方法在痳醉雄性大鼠隔離灌流頸動脈竇區條件下記錄竇神經傳入放電及積分.結果① CCK-8 0.1,0.5和1.0 μmol·L-1使壓力感受器機能麯線嚮右下方移位,麯線最大斜率和竇神經傳入放電積分最大值均明顯減小,錶明CCK-8可劑量依賴性抑製頸動脈竇壓力感受器活動.②預先灌流CCK-8非特異性受體阻斷劑丙穀胺100 μmol·L-1或鈣通道開放劑Bay K8644 0.5 μmol·L-1可部分阻斷CCK-8 0.5 μmol·L-1對頸動脈竇壓力感受器放電活動的抑製作用.預先灌流一氧化氮閤酶抑製劑L-NAME不能阻斷CCK-8的效應.結論 CCK-8可直接抑製大鼠頸動脈竇壓力感受器傳入神經放電活動.其機製可能為CCK-8作用于頸動脈竇區相應的受體後,對牽張敏感性通道產生抑製作用.
목적관찰팔태담낭수축소(CCK-8)시부통과직접억제경동맥두압력감수기방전활동이영향심혈관공능.방법재마취웅성대서격리관류경동맥두구조건하기록두신경전입방전급적분.결과① CCK-8 0.1,0.5화1.0 μmol·L-1사압력감수기궤능곡선향우하방이위,곡선최대사솔화두신경전입방전적분최대치균명현감소,표명CCK-8가제량의뢰성억제경동맥두압력감수기활동.②예선관류CCK-8비특이성수체조단제병곡알100 μmol·L-1혹개통도개방제Bay K8644 0.5 μmol·L-1가부분조단CCK-8 0.5 μmol·L-1대경동맥두압력감수기방전활동적억제작용.예선관류일양화담합매억제제L-NAME불능조단CCK-8적효응.결론 CCK-8가직접억제대서경동맥두압력감수기전입신경방전활동.기궤제가능위CCK-8작용우경동맥두구상응적수체후,대견장민감성통도산생억제작용.
AIM To study if cholecystokinin octapeptide (CCK-8) alter cardiovascular functions by its direct inhibitory effect on carotid sinus baroreceptor (CSB) activity. METHODS The functional curve of carotid baroreceptor (FCCB) was constructed and the functional parameters of carotid baroreceptor were measured by recording sinus nerve afferent discharge in anesthetized male rats with perfused isolated carotid sinus. RESULTS ① CCK-8 0.1, 0.5 and 1.0 μmol·L-1 shifted FCCB to the right and downward, with a marked decrease in peak slope and peak integral value of carotid sinus nerve discharge in a concentration-dependent manner, indicating the inhibitory effect of CCK-8 on CSB activity. ② Pretreatment with proglumide (100 μmol·L-1), a nonselective CCK receptor antagonist, or Bay K8644 (0.5 μmol·L-1), an agonist of calcium channel, partially attenuated the inhibitory effect of CCK-8 (0.5 μmol·L-1) on CSB activity. Pretreatment with L-NAME (100 μmol·L-1), an inhibitor of NO synthase, did not affect the inhibitory action of CCK-8. CONCLUSION CCK-8 inhibits CSB activity, which may be mediated by activating CCK receptors in the carotid sinus area and thereby resulting in an inhibition of stretch-sensitive channels and decrease in Ca2+ influx.
