Paterson D J, Rogers J, Powell T, Brown H F
University Laboratory of Physiology, Oxford, UK.
Acta Physiol Scand. 1993 Jun;148(2):177-86. doi: 10.1111/j.1748-1716.1993.tb09547.x.
We describe the relationship between catecholamines and raised extracellular potassium ([K+]o) on action potential parameters and calcium currents in isolated ventricular myocytes of the guinea-pig and relate these findings to the problem of understanding how the heart is protected from exercise-induced hyperkalaemia ([K+]a up to 8.5 mM). Action potential duration (APD90), amplitude and upstroke velocity were recorded in stimulated (2Hz) guinea-pig ventricular myocytes using whole-cell patch electrode recordings (37 degrees C). Cells were superfused with normal K+ Tyrode and with raised K+ Tyrode in the presence of either noradrenaline, adrenaline or raised calcium. Inward calcium current was measured using voltage clamp. Raised K+ (8, 12, 16 mM K+ Tyrode) caused a significant (P < 0.01) depolarisation, shortened the APD90 and decreased the action potential amplitude and upstroke velocity. In raised K+ Tyrode addition of noradrenaline (0.08-0.1 microM) or adrenaline (0.1-0.2 microM) increased action potential amplitude (P < 0.01), APD90 (P < 0.01) and upstroke velocity (P < 0.01) (measured only in 16 mM K+ Tyrode). In 12 mM K+ Tyrode raised Ca2+ (5-6 mM) increased action potential amplitude (P < 0.05) and shortened APD90 (P < 0.05). Addition of NA (0.08-0.1 microM) increased the inward Ca2+ current. All effects were fully reversible. In raised [K+]o increases in catecholamines and [Ca2+]o cause changes in action potential parameters that would be expected to maintain propagation of the cardiac action potential in the whole heart. Thus, in the ventricular myocyte the increase in conductance to Ca2+ caused by catecholamines may be one factor that is important in minimising the potentially adverse effects of exercise-induced hyperkalaemia.
我们描述了儿茶酚胺与细胞外钾离子浓度升高（[K⁺]o）对豚鼠离体心室肌细胞动作电位参数和钙电流的影响，并将这些发现与理解心脏如何免受运动诱导的高钾血症（[K⁺]a高达8.5 mM）的问题联系起来。使用全细胞膜片钳记录（37℃）在刺激（2Hz）的豚鼠心室肌细胞中记录动作电位持续时间（APD90）、幅度和上升速度。细胞用正常钾离子的台氏液以及在去甲肾上腺素、肾上腺素或钙离子浓度升高的情况下用升高钾离子的台氏液进行灌流。使用电压钳测量内向钙电流。升高的钾离子（8、12、16 mM钾离子的台氏液）导致显著（P < 0.01）的去极化，缩短了APD90，并降低了动作电位幅度和上升速度。在升高钾离子的台氏液中加入去甲肾上腺素（0.08 - 0.1 μM）或肾上腺素（0.1 - 0.2 μM）可增加动作电位幅度（P < 0.01）、APD90（P < 0.01）和上升速度（仅在16 mM钾离子的台氏液中测量，P < 0.01）。在12 mM钾离子的台氏液中升高钙离子浓度（5 - 6 mM）可增加动作电位幅度（P < 0.05）并缩短APD90（P < 0.05）。加入去甲肾上腺素（0.08 - 0.1 μM）可增加内向钙电流。所有效应都是完全可逆的。在[K⁺]o升高时，儿茶酚胺和[Ca²⁺]o的增加会导致动作电位参数的变化，这有望维持心脏动作电位在整个心脏中的传播。因此，在心室肌细胞中，儿茶酚胺引起的钙离子电导增加可能是最小化运动诱导的高钾血症潜在不利影响的一个重要因素。
