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目的探讨钩藤碱(Rhy)对大鼠颈动脉窦压力感受器活动的影响及其有关机制。方法通过隔离灌流颈动脉窦区的方法来获得颈动脉窦压力感受器活动的各项参数,阈压(TP)、饱和压(SP)、最大斜率(PS)和窦神经放电的最大积分值(PIV)。① Rhy10, 50和100μmo·lL-1用K-H液稀释后,隔离灌流颈动脉窦区。待钩藤碱发挥作用后,用K-H液冲洗恢复,在给药前后以阶梯方式升降窦内压以刺激颈动脉窦压力感受器,同时记录窦神经传入放电及积分。②分别预先灌流一氧化氮合酶抑制剂左旋硝基精氨酸甲酯(L-NAME)、K+通道阻断剂四乙胺(TEA)和L-钙通道开放剂Bay K8644,观察他们对钩藤碱效应的影响。结果①Rhy 10μmol.L-1灌流隔离的颈动脉窦区,PS从(19.2±0.3)%降至(18.2±0.1)%·kPa-1,PIV从(219.3±3.3)%降至(199.1±3.8)%,同时TP和SP分别从(8.2±0.3)和(21.5±0.1)增加至(9.1±0.1)kPa和(22.1±0.1)kPa。用Rhy 50和100μmol·L-1进行灌流时,如PS,TP和SP的变化均呈浓度依赖性,表明Rhy可以抑制CBA。②预先灌流L-NAME不能阻断Rhy的效应。③预先灌流K+通道阻断剂TEA 1mmol·L-1也不能阻断Rhy对颈动脉窦压力感受器放电活动的抑制。④预先灌流L-钙通道开放剂Bay K8644可大部分阻断Rhy的作用。结论 Rhy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Rhy抑制了动脉压力感受器上的Ca2+内流。
Objective To investigate the effect of rhychine on rat carotid sinus baroreceptor activity and its related mechanisms. Methods Parameters of carotid sinus baroreceptor activity were obtained by isolating the perfused carotid sinus region, and the maximum integral value of the threshold pressure (TP), saturation pressure (SP), maximum slope (PS) and sinus nerve discharge (PIV). ). 1 Rhy10, 50 and 100 μmol·L-1 were diluted with K-H solution and perfused with carotid sinus. After rhynchophylline had a role, it was rinsed with K-H solution. Before and after administration, sinus pressure was raised and lowered in a step manner to stimulate carotid sinus baroreceptors. At the same time, sinus nerve afferent discharges and scores were recorded. 2 Pre-perfused with nitric oxide synthase inhibitor L-nitro-L-arginine methyl ester (L-NAME), K+ channel blocker tetraethylammonium (TEA) and L-calcium channel opener Bay K8644 respectively, observe their hooks Effect of the rattanine effect. Results 1Rhy 10μmol.L-1 perfused isolated carotid sinus region, PS decreased from (19.2±0.3)% to (18.2±0.1)%·kPa-1, and PIV decreased from (219.3±3.3)% to (199.1±3.8). )%, while TP and SP increased from (8.2 ± 0.3) and (21.5 ± 0.1) to (9.1 ± 0.1) kPa and (22.1 ± 0.1) kPa, respectively. When perfusion was performed with Rhy 50 and 100 μmol·L-1, the changes of PS, TP and SP were concentration-dependent, indicating that Rhy could inhibit CBA. 2 Pre-perfusion of L-NAME does not block Rhy’s effect. 3 Pre-perfusion of the K+ channel blocker TEA 1 mmol·L-1 did not block Rhy’s inhibition of carotid sinus baroreceptor discharge activity. 4 The pre-perfused L-calcium channel opener Bay K8644 can largely block Rhy’s effect. Conclusion Rhy can directly inhibit the activity of afferent nerves in rat carotid sinus baroreceptors. The mechanism may be that Rhy inhibits Ca2+ influx on arterial baroreceptors.