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目的:研究粉防己碱对培养乳牛基底动脉平滑肌细胞游离钙浓度([Ca2+]i)的影响.方法:利用AR-CM-MIC阳离子测定系统,采用Fura 2-AM为指示剂,测量单个细胞内[Ca2+]i.结果:粉防己碱10-100μmol/L对培养乳牛基底动脉平滑肌细胞静息[Ca2+]i无明显影响.在细胞外钙为1.3 mmol/L,粉防己碱可浓度依赖性地抑制KCl引起[Ca2+]i的升高.咖啡因10 mmol/L可诱导一次[Ca2+]i瞬间快速升高,随后自发回复到静息水平.粉防己碱10和30 μmol/L对咖啡因诱导的[Ca2+]i瞬间升高没有作用,但高浓度(100μmol/L)粉防己碱抑制了[Ca2+]i瞬间升高.在细胞外钙为1.3 mmol/L,苯肾上腺素10 μmol/L可引起双相[Ca2+]i变化,包括快速升高相和持续升高相.在细胞外钙为零,苯肾上腺素仅引起[Ca2+]i的快速升高相.粉防己碱可浓度依赖性地抑制苯肾上腺素引起[Ca2+]i的持续升高相.但仅高浓度粉防己碱明显抑制了[Ca2+]i快速升高相.结论:在培养乳牛基底动脉平滑肌细胞,粉防己碱可能通过影响电压依赖性和苯肾上腺素受体介导的钙通道而抑制钙内流.高浓度粉防己碱也可能影响肌浆网钙释放或钙摄取.“,”AIM: To study the effects of tetrandrine (Tet) on extracellular Ca2+ influx and intracellular Ca2+ release in cultured calf basilar artery smooth muscle cells. METHODS: Free intracellular calcium was examined by a system of measurement of AR-CM-MIC, using Fura 2-AM as a fluorescent indicator. RESULTS: In the presence of extracellular Ca2+ 1.3 mmol/L, no significant effect of Tet on resting [Ca2+]i was found. KCl 20, 40, and 60 mmol/L triggered a sustained rise in [Ca2+]i, pretreatment with Tet inhibited the elevation of [Ca2+]i induced by KCl in concentration-dependent manner, Tet at high concentration (100 μmol/L) almost abolished the rise of [Ca2+]i evoked by KCl. Caffeine 10 mmol/L only produced a transient increase of [Ca2+]i, which spontaneously declined back to resting levels. Tet 10-30 μmol/L had no effect on caffeine-induced [Ca2+]i transient peak. Tet at high concentration (100 μtmol/L), however, reduced the [Ca2+]i transient peak induced by caffeine. Phenylephrine (PE) 10 mmol/L produced a rapid transient peak and a distinct sustained elevation in [Ca2+]i in the presence of extracellular Ca2+. In the absence of extracellular Ca2+ containing egtazic acid (EGTA), PE only produced a rapid transient peak in [Ca2+]i. Pretreatment of Tet (10-100 μmol/L) inhibited the sustained elevation in [Ca2+]i induced by PE in a concentration-dependent manner. However, only 100 μmol/L of Tet inhibited the transient peak in [Ca2+]i induced by PE both in the presence of extracellular Ca2+ 1.3 mmol/L and in the absence of extracellular Ca2+ containing EGTA.CONCLUSION: Tet inhibited the Ca2+ influx from the extracellular site via voltage-activated Ca2+ channel and PE-receptor-operated Ca2+ channel. At a high concentration, Tet may inhibit the Ca2+ release from sarcoplasmic reticulum (SR) or refilling of intracellular calcium store in cerebral artery smooth muscle cells.