Viko H, Osnes J B, Skomedal T
Department of Pharmacology, University of Oslo, Norway.
Res Commun Mol Pathol Pharmacol. 1997 Apr;96(1):89-106.
The aim of the present study was to identify the mechanism(s) responsible for the alpha 1-adrenoceptor stimulated increase in potassium uptake in ventricular cardiomyocytes isolated from adult rat heart. The Na+/K+ATPase blocker ouabain the Na+/K+/2Cl(-)-cotransporter blocker bumetanide, the Na+/H(+)-exchanger blocker HOE 694 and the potassium channel blocker 4-aminopyridine were used as experimental tools. 86Rb+ was used as potassium analogue. The basal 86Rb(+)-uptake rate was 0.25 +/- 0.01 ml/g protein x min. Maximal alpha 1-adrenoceptor stimulation increased the 86Rb(+)-uptake 38 +/- 2%. Ouabain dose dependently eliminated the alpha 1-adrenoceptor stimulated response with a -logIC50-value of 3.64 +/- 0.23. Bumetanide did not affect the stimulated response, and there was no effect of bumetanide on the ouabain sensitive component. HOE 694 and 4-aminopyridine had no effect on the stimulated 86Rb(+)-uptake. Ouabain and HOE 694 also dose dependently inhibited a portion of the basal 86Rb(+)-uptake (about 60% and 20%, respectively), but there was no effect of bumetanide or 4-aminopyridine on the basal 86Rb(+)-uptake. The results show that the Na+/K+ATPase alone mediates the alpah 1-adrenoceptor stimulated increase in potassium uptake in this preparation of ventricular cardiomyocytes isolated from adult rat heart.
本研究的目的是确定成年大鼠心脏分离的心室心肌细胞中,α1肾上腺素能受体刺激钾摄取增加的机制。使用钠钾ATP酶阻滞剂哇巴因、钠钾氯共转运体阻滞剂布美他尼、钠氢交换体阻滞剂HOE 694和钾通道阻滞剂4-氨基吡啶作为实验工具。86Rb+用作钾的类似物。基础86Rb+摄取率为0.25±0.01 ml/g蛋白质×分钟。最大α1肾上腺素能受体刺激使86Rb+摄取增加38±2%。哇巴因剂量依赖性地消除α1肾上腺素能受体刺激的反应,-logIC50值为3.64±0.23。布美他尼不影响刺激反应,且对哇巴因敏感成分无影响。HOE 694和4-氨基吡啶对刺激的86Rb+摄取无影响。哇巴因和HOE 694也剂量依赖性地抑制一部分基础86Rb+摄取(分别约为60%和20%),但布美他尼或4-氨基吡啶对基础86Rb+摄取无影响。结果表明,在这种成年大鼠心脏分离的心室心肌细胞制剂中,单独的钠钾ATP酶介导α1肾上腺素能受体刺激的钾摄取增加。