Wakabayashi I, Sakamoto K, Kakishita E
Second Department of Internal Medicine, Hyogo College of Medicine, Japan.
J Pharm Pharmacol. 1990 Oct;42(10):716-9. doi: 10.1111/j.2042-7158.1990.tb06566.x.
The effects of daunorubicin on vasoconstraction by several agonists have been investigated on isolated aortic strips from rats. Pretreatment of the strips with daunorubicin (17.7 microM) potentiated the contractile response to low concentrations of KCl or to BAY K 8644 but not to phenylephrine or clonidine. The maximal contractile response to KCl was not affected by the pretreatment while that to BAY K 8644 was increased. The potentiated response to KCl could be eliminated by addition of nifedipine (1 microM) or use of a calcium-free solution. The maximal contractile response to BAY K 8644 was greatly increased by partial depolarization with KCl (10 mM, final concn) in the control solution but only slightly increased by the partial depolarization in the solution with daunorubicin. These results suggest that daunorubicin facilitates activation of the voltage-dependent calcium channel and increases the contractile responses to KCl and BAY K 8644 in rat aorta.
已经在大鼠离体主动脉条上研究了柔红霉素对几种激动剂引起的血管收缩的影响。用柔红霉素(17.7微摩尔)预处理主动脉条可增强对低浓度氯化钾或BAY K 8644的收缩反应,但对去氧肾上腺素或可乐定则无此作用。对氯化钾的最大收缩反应不受预处理影响,而对BAY K 8644的最大收缩反应则增强。加入硝苯地平(1微摩尔)或使用无钙溶液可消除对氯化钾增强的反应。在对照溶液中用氯化钾(最终浓度10毫摩尔)进行部分去极化可使对BAY K 8644的最大收缩反应大大增强,但在含有柔红霉素的溶液中进行部分去极化时,该反应仅略有增加。这些结果表明,柔红霉素促进电压依赖性钙通道的激活,并增加大鼠主动脉对氯化钾和BAY K 8644的收缩反应。