Toda N
J Cardiovasc Pharmacol. 1982 May-Jun;4(3):469-74. doi: 10.1097/00005344-198205000-00019.
In helical strips of dog cerebral arteries soaked in Ca2+-free media and treated with prostaglandin (PG) F2 alpha or K+, the addition of Ca2+ produced a transient contraction, transient relaxation, and slowly developing, persistent contraction. Treatment with 2 X 10(-7) M ouabain did not alter the contractile response to PGF2 alpha in Ca2+-free media, but potentiated the response to Ca2+. Relaxations following the transient contractions were abolished by ouabain. On the other hand, ouabain potentiated the contractile response to serotonin in Ca2+-free media, and also the response to Ca2+. In mesenteric arterial strips soaked in Ca2+-free media, ouabain at 2 X 10(-7) M insufficient to produce contractions increased the contractile response to Ca2+, and the increase in the concentration to 2 X 10(-5) M potentiated the response to PGF2 alpha and serotonin. It may be concluded that ouabain increases the influx of Ca2+ across cell membrane caused by vasoconstrictors and enhances the drug-induced release of Ca2+ from intracellular storage sites.
在浸泡于无钙培养基并用前列腺素(PG)F2α 或钾处理的犬脑动脉螺旋条中,加入钙离子会产生短暂收缩、短暂舒张以及缓慢发展的持续性收缩。用2×10⁻⁷ M哇巴因处理并不会改变无钙培养基中对PGF2α 的收缩反应,但会增强对钙离子的反应。哇巴因可消除短暂收缩后的舒张反应。另一方面,哇巴因会增强无钙培养基中对5-羟色胺的收缩反应,以及对钙离子的反应。在浸泡于无钙培养基的肠系膜动脉条中,2×10⁻⁷ M的哇巴因不足以产生收缩,但会增加对钙离子的收缩反应,将浓度提高到2×10⁻⁵ M会增强对PGF2α 和5-羟色胺的反应。可以得出结论,哇巴因会增加血管收缩剂引起的钙离子跨细胞膜内流,并增强药物诱导的细胞内储存部位钙离子释放。