Ellingsen O, Sejersted O M, Vengen O A, Ilebekk A
Institute for Experimental Medical Research, University of Oslo, Norway.
Acta Physiol Scand. 1989 Apr;135(4):493-503. doi: 10.1111/j.1748-1716.1989.tb08608.x.
Maintenance of adequate electrical activity of the heart depends critically on the ability of the Na-K pump to compensate for normal passive sodium and potassium fluxes. Using sudden injections of [3H]ouabain into the left coronary artery in anaesthetized open-chest pigs, we monitored transient changes in myocardial potassium balance by PVC-valinomycin mini-electrodes. When related to the number of pumps blocked and fractional inhibition, these data provided estimates of total Na-K pump capacity as well as actual pump rate and perturbations of the Na-K balance. Experiments were performed in hearts with and without intracoronary isoprenaline infusion (2.5 nmol min-1). After injection of 120 nmol [3H]ouabain into the left coronary artery, myocardial [3H]ouabain concentrations were 118 (74-178) and 103 (76-145) pmol g-1 and total concentrations of [3H]ouabain binding sites were 893 (752-1076) and 785 (691-877) pmol g-1 (median, 95% confidence interval) in isoprenaline-treated and control hearts respectively (differences not significant). The [3H]ouabain injection caused a net potassium release of 81 (56-132) and 43 (23-75) mumol 100 g-1 (median, 95% confidence interval) in isoprenaline-treated and control hearts respectively (n = 6-8; significance of difference, P = 0.03). Na-K pump rate estimated from mono-exponential release curves was 6363 (3942-10,858) K+ ions min-1 site-1 during beta-adrenoceptor stimulation and 2514 (1380-4322) in control (significance of difference, P = 0.03). This corresponds to 40 and 16%, respectively, of the maximum possible pump rate determined from ATP hydrolysis. Comparison of accumulated potassium release and relative Na-K pump rate indicates that catecholamines enhance the sensitivity of the Na-K pump for intracellular sodium.
心脏维持充足的电活动关键取决于钠钾泵补偿正常被动钠钾通量的能力。我们通过向麻醉开胸猪的左冠状动脉突然注射[³H]哇巴因，使用聚氯乙烯 - 缬氨霉素微型电极监测心肌钾平衡的瞬时变化。当与被阻断的泵数量和部分抑制相关时，这些数据提供了钠钾泵总容量、实际泵速率以及钠钾平衡扰动的估计值。实验在有和没有冠状动脉内输注异丙肾上腺素（2.5 nmol·min⁻¹）的心脏中进行。向左冠状动脉注射120 nmol [³H]哇巴因后，异丙肾上腺素处理的心脏和对照心脏的心肌[³H]哇巴因浓度分别为118（74 - 178）和103（76 - 145）pmol·g⁻¹，[³H]哇巴因结合位点的总浓度分别为893（752 - 1076）和785（691 - 877）pmol·g⁻¹（中位数，95%置信区间）（差异不显著）。[³H]哇巴因注射在异丙肾上腺素处理的心脏和对照心脏中分别引起100 g⁻¹心肌净钾释放81（56 - 132）和43（23 - 75）μmol（中位数，95%置信区间）（n = 6 - 8；差异显著性，P = 0.03）。根据单指数释放曲线估计的钠钾泵速率在β - 肾上腺素能受体刺激期间为6363（3942 - 10858）K⁺离子·min⁻¹·位点⁻¹，对照中为2514（1380 - 4322）（差异显著性，P = 0.03）。这分别相当于根据ATP水解确定的最大可能泵速率的40%和16%。累积钾释放与相对钠钾泵速率的比较表明，儿茶酚胺增强了钠钾泵对细胞内钠的敏感性。
