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本文运用fura-2技术研究了K~+通道阻滞剂对Carbacol(氨甲酰胆碱)介导的Ca~(2+)进入人类排Cl~-的HT-29/B6并影响胞内钙浓度的作用。结果表明,用100μmol/L氨甲酰胆碱刺激HT-29/B6可产生清晰的双相Ca~(2+)反应:Ca从静息水平(85±3nmol/L)迅速激发至短暂的峰值(821±44nmol/L),随后降至一段平台(317±12nmol/L)。平台高度与胞外Ca~(2+)浓度相关并在Ca~(2+)出入胞浆膜之间代表着新的平衡状态。平台在缺Ca~(2+)的条件下不出现而钙峰无论在有钙或无钙条件下均能出现,这表明Ca~(2+)峰的出现是由胞内Ca~(2+)库释放所致,而平台的维持则是外钙流入胞内所致。加阿托品
Fura-2 was used to study the effects of K ~ + channel blockers on Carbacol-mediated Ca ~ (2+) entry into HT-29 / B6 cells and the effect of intracellular calcium Concentration effect. The results showed that the stimulation of HT-29 / B6 with 100 μmol / L carbachol gave a clear biphasic Ca 2+ response: Ca was rapidly excited from resting level (85 ± 3 nmol / L) to transient peak (821 ± 44 nmol / L) and then decreased to a plateau (317 ± 12 nmol / L). The height of the platform correlates with the extracellular Ca 2+ concentration and represents a new equilibrium between the Ca 2+ entry and exit of the cytoplasm. The platform does not appear in the absence of Ca ~ (2+) and the calcium peak appears in both Ca ~ (2+) and Ca ~ (2+) - free conditions, indicating Ca ~ (2+) ) Library release caused by the platform to maintain the external calcium influx caused due. Add atropine