P型Ca^(2+)通道在高K^(+)引起的大鼠小脑一氧化氮合酶激活中作用  

THE ROLE OF P-TYPE CALCIUM CHANNELS IN THE K^(+)-INDUCED ACTIVATION OF NITRIC OXIDE SYNTHAS IN RAT CEREBELLUM

作　　者：金英[1] 赵艳杰[1] 焦金菊[2] 张宝云 

机构地区：[1]锦州医学院药理教研室 [2]锦州医学院生理教研室 [3]锦州药业器化玻有限公司

出　　处：《锦州医学院学报》2000年第5期1-4,共4页Journal of Jinzhou Medical College

摘　　要：目的 :用大鼠小脑脑片研究 P型 Ca2 +通道在高 K+引起的一氧化氮合酶激活中作用。方法 :通过测定 L-[3H]精氨酸转变成 L-[3H]瓜氨酸来判定一氧化氮合酶 ( NOS)活性。结果 :表明 50 mmol· L- 1 K+可明显提高 NOS活性。特异性 P型钙通道阻断剂蜘蛛毒素 AGA 0 .1 nmmol· L- 1 和蜘蛛毒素FTX1 0 0 nmmol· L- 1可以明显阻断 50 mmol· L- 1 K+引起 NOS活性增强作用。NMDA受体通道阻断剂 MK-80 1 1 0 nmmol·L- 1不能阻断 50 mmol·L- 1 K+引起 NOS活性增强作用。结论 :说明高 K+引起 NOS活性增强主要是由于 Ca2 +通过 P型钙通道进入细胞内引起的。谷氨酸受体不参与高 K+引起Objective:The role of P type calcium channels in the K + induced activation of nitric oxide synthas was studied in rat cerebeller slices.Methods:Nitric oxide systhase(NOS) activity was determined by measuring the conversion of L [ 3H]arginine to L [ 3H]citrulline.Results:In this study ,we demonstrate that K + at 50 mmol·L -1 enhanced the conversion of L [ 3H]arginine to L [ 3H]citrulline.This enhanced activity was obviously blocked by the selective inhibitor of P type calcium channels(AGA 0.1 nmol·L -1 and FTX 100 nmol·L -1 .However,MK 801,a non competitive NMDA antagonist was ineffective in blocking the response to 50 mmol·L -1 K +.Conclusion:These results suggest that the stimulation of NOS by K + is due to influx of calcium through the P type channel and that the NMDA receptor is not involved in the activity of NOS by K +.

关 键 词：氯化钾 P-型钙通道 一氧化氮合酶 小脑 

分 类 号：R338[医药卫生—人体生理学]