哇巴因诱导的人胎盘血管收缩中的钠/钙交换介导作用

Na+/Ca2+ exchange mediation in the ouabain-induced contraction in human placental vessels.

Fernández-Alfonso M S, Sánchez-Ferrer C F, Hernández M C, Marín J

Departamento de Farmacología y Terapéutica, Facultad de Medicina, Universidad Autónoma, Madrid, Spain.

Gen Pharmacol. 1992 May;23(3):439-44. doi: 10.1016/0306-3623(92)90109-w.

Abstract

Ouabain induced concentration-dependent contractions in segments of human placental arteries and veins, which were practically abolished in a Ca(2+)-free medium and not modified by the calcium antagonist nifedipine or the calcium agonist Bay K 8644. 2. Ouabain (10(-4) M) elicited a time-dependent enhancement of the 45Ca2+ uptake, which remained equal in presence of nifedipine or Bay K 8644. 3. The Na+/Ca2+ exchange blocker amiloride reduced both the contractions and the 45Ca2+ uptake induced by ouabain, whereas the Na ionophore monensin produced a parallel shift to the left of the concentration-response curve to ouabain. 4. These results suggest that ouabain-induced contractions in these vessels are dependent on the extracellular Ca2+, which mainly enters into the cell through the Na+/Ca2+ exchange system.

摘要

哇巴因可引起人胎盘动脉和静脉段浓度依赖性收缩，在无钙培养基中这种收缩几乎完全消失，且不受钙拮抗剂硝苯地平或钙激动剂Bay K 8644的影响。2. 哇巴因（10⁻⁴ M）可引起45Ca²⁺摄取的时间依赖性增强，在硝苯地平或Bay K 8644存在时该摄取量保持不变。3. Na⁺/Ca²⁺交换阻滞剂阿米洛利可减少哇巴因诱导的收缩和45Ca²⁺摄取，而Na离子载体莫能菌素使哇巴因浓度-反应曲线向左平行移动。4. 这些结果表明，哇巴因在这些血管中诱导的收缩依赖于细胞外Ca²⁺，其主要通过Na⁺/Ca²⁺交换系统进入细胞。