Garay R P, Diez J, Nazaret C, Dagher G, Abitbol J P
Naunyn Schmiedebergs Arch Pharmacol. 1985 May;329(3):311-5. doi: 10.1007/BF00501886.
Canrenone inhibits 30-40% of ouabain-sensitive Na+ efflux in human red cells. Half-maximal inhibition was obtained with a canrenone concentration = 86 +/- 37 mumol/l (mean +/- SD of 13 experiments). The partial inhibition of the Na+,K+ pump appears to be mediated at the digitalis receptor site with an apparent dissociation constant (Kc) = 200 +/- 130 mumol/l (mean +/- SD). Further evidence suggesting that canrenone is a partial agonist at the digitalis receptor site was obtained by the observation that it decreases the apparent affinity of the Na+,K+ pump for external K+. However, in contrast to ouabain, canrenone decreases the apparent pump affinity for internal Na+. Our results show that, at physiological cell Na+ levels canrenone is able to enhance the inhibition of the Na+,K+ pump by low doses of ouabain. Conversely, in cells treated with high concentrations of cardiac glycosides (in which cell Na+ content increases), canrenone is able to restimulate the blocked pumps.
坎利酮可抑制人红细胞中约30 - 40%的哇巴因敏感的Na⁺外流。当坎利酮浓度为86±37 μmol/L（13次实验的平均值±标准差）时可获得半数最大抑制。Na⁺,K⁺泵的部分抑制似乎是在洋地黄受体位点介导的，表观解离常数（Kc）为200±130 μmol/L（平均值±标准差）。通过观察到坎利酮降低了Na⁺,K⁺泵对细胞外K⁺的表观亲和力，获得了进一步证据表明坎利酮是洋地黄受体位点的部分激动剂。然而，与哇巴因不同，坎利酮降低了泵对细胞内Na⁺的表观亲和力。我们的结果表明，在生理细胞Na⁺水平下坎利酮能够增强低剂量哇巴因对Na⁺,K⁺泵的抑制作用。相反，在用高浓度强心苷处理的细胞中（其中细胞Na⁺含量增加），坎利酮能够重新刺激被阻断的泵。
