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作 者:徐济良[1] 杨毓麟[1] 关永源[1] 孙家钧[1]
机构地区:[1]南通医学院药理教研室,广州中山医科大学药理教研室
出 处:《中国药理学通报》1996年第1期59-61,共3页Chinese Pharmacological Bulletin
摘 要:萘甲异喹(NI1,10μmol·L-1)和硝苯吡啶(Nif0.5μmol·L-1)对大鼠主动脉平滑肌45Ca溢流无影响,NI(1~30μmol·L-1)能浓度依赖地抑制高钾和苯肾上腺素引起的大鼠主动脉平滑肌45Ca内流,抑制率分别为27%~81%和17%~77%,NI(10μmol·L-1)尚可明显抑制由苯肾上腺素引起的45Ca外溢。这些结果提示NI能抑制平滑肌细胞膜PDC和ROC两类钙通道及细胞内钙释放。The effects of naphthylmethyl isoquinoline(NI)on 45Ca flux of vascular smooth muscle in rat aorta were studied in comparison with nifedipine(Nif).NI(1,10 μmol·L-)andNif(0.5 μmol· L-1)had no effect on the resting 45Ca leak in rat aorta.NI(1~30 μmol·L-1)could decrease the45Ca influx of rat aorta induced by KCI(100 mmol·L-1)and phenylephrine(PHE 10μmol·L-1)in the concentration dependent manner.The rates of inhibition were 27%~81% and 17%~77% respectively. The effects of NI were less in potency than ones of Nif. NI(10μmol· L-1)could markedly inhibite 45Ca efflux induced by PHE(10μmol·L-1).The results indicated that NI had nonselective blocking effect between potential dependent Ca2+channels and receptor operated Ca2+ channels,and could inhibit Ca2+ release from intracellular calcium storage site.
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