Shimizu I, Toda N
Jpn J Pharmacol. 1986 Feb;40(2):257-63. doi: 10.1254/jjp.40.257.
Contractile responses to ouabain in helical strips of dog and monkey coronary arteries were investigated. Ouabain (5 X 10(-8) to 5 X 10(-6) M) caused a dose-related contraction in dog and monkey arteries; the response of monkey coronary arteries was significantly greater. In dog coronary arteries, contractile responses to high concentrations of ouabain were potentiated by treatment with propranolol. In the arteries contracted with ouabain, the addition of phentolamine caused a relaxation. Contractile responses of dog coronary arteries to ouabain were markedly suppressed by exposure to Ca2+-free media or by treatment with verapamil. Reduction of external concentration of K+ or lowering the temperature of bathing media did not selectively influence the ouabain-induced contraction. These results suggest that ouabain-induced contractions of dog coronary arteries are associated mainly with an increase in the Ca2+-influx, which does not result from an inhibition of the Na+, K+-activated ATPase nor from an activation of alpha adrenoceptors by noradrenaline released from adrenergic nerves. Ouabain in high concentrations seems to liberate noradrenaline from adrenergic nerves, which preferentially activates beta adrenoceptors in dog coronary artery.
研究了哇巴因对犬和猴冠状动脉螺旋条的收缩反应。哇巴因(5×10⁻⁸至5×10⁻⁶M)可引起犬和猴动脉剂量相关的收缩;猴冠状动脉的反应明显更大。在犬冠状动脉中,普萘洛尔处理可增强对高浓度哇巴因的收缩反应。在用哇巴因收缩的动脉中,加入酚妥拉明可引起舒张。暴露于无钙培养基或用维拉帕米处理可明显抑制犬冠状动脉对哇巴因的收缩反应。降低细胞外钾离子浓度或降低浴液温度不会选择性地影响哇巴因诱导的收缩。这些结果表明,哇巴因诱导的犬冠状动脉收缩主要与钙离子内流增加有关,这既不是由于钠钾激活的ATP酶受到抑制,也不是由于肾上腺素能神经释放的去甲肾上腺素激活α肾上腺素受体所致。高浓度的哇巴因似乎能从肾上腺素能神经中释放去甲肾上腺素,而去甲肾上腺素优先激活犬冠状动脉中的β肾上腺素受体。