The combination of whole-cell patch clamp and fura-2 fluorescence techniques had been used to investigate the ATP-activated Cl- current and Ca2+ entry in bovine aortic endothelial cells (BAEC). Application of ATP activated an outward current. The I-V curve showed pronounced outward rectification and the current reversed at －(29±3)mV, which was close to the equilibrium potential for Cl- (－36 mV). Reducing the ［Cl-］o caused a shift in the reversal potential towards more positive potentials. It indicated that the ATP-activated current was mainly carried by Cl-. ATP-activated Cl- current was ［Ca2+］i dependent, it was maximally inhibited by Cl- channel blockers furosemide and glibenclamide with (88±8)% and (93±4)% at +100 mV. Application of ATP activated Ca2+ influx from the extracellular space. ATP-induced Ca2+ entry was inhibited by furosemide and glibenclamide with (36±14)% and (44±12)%, respectively. The Ca2+ influx sensitive to furosemide is not the same as that to glibenclamide. These observations suggest that opening of Cl- channel plays an important role in the regulation of Ca2+ entry in BAEC.%采用全细胞膜片钳技术和fura-2荧光测定胞浆［Ca2+］i变化技术，在培养的牛主动脉内皮细胞上观察ATP诱导的Cl-电流的特性及其与Ca2+内流的关系。记录到ATP激活一外向电流，其反转电位为－(29±8)mV，与Cl-的平衡电位接近，降低细胞外Cl-浓度使反转电位变化，证明是Cl-电流. ATP激活的Cl-电流具有较强的外向整流特性，具有Ca2+依赖性，可被Cl-通道阻滞剂呋塞米和格列本脲分别最大抑制(88±8)%和(93±4)%（+100 mV）. ATP又可诱导内皮细胞外Ca2+内流，呋塞米和格列本脲对Ca2+内流分别最大抑制(36±14)%和(44±12)%，并且二者敏感的Ca2+内流特性不同. 结果说明Cl-通道开放在调节内皮细胞Ca2+内流中起重要作用.
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