Ryan D M, Paterson D J
University Laboratory of Physiology, Oxford, UK.
Acta Physiol Scand. 1996 Apr;156(4):419-27. doi: 10.1046/j.1365-201X.1996.453213000.x.
Catecholamines restore cardiac contraction depressed by hyperkalaemia (raised [K+]O) and acidosis, yet in exercise hyperkalaemia and acidosis are tolerated during beta adrenergic blockade. To test whether the negative effects of raised [K+]O are offset by a non-adrenergic hormone, angiotensin II (AII) was given to rabbit papillary muscle (All 75 nM, n = 9) and rabbit isolated working hearts (All 5 nM, n = 8) perfused with 8 and 10 mM K+ Tyrode at 37 degrees C. A similar protocol was also performed in a further nine isolated hearts treated with propranolol (1 microM) and prazosin (1 microM). All caused a significant (P < 0.01) increases in contraction and aortic flow in normal Tyrode and maintained aortic flow during high [K+]O. In the papillary muscle and isolated heart treated with adrenergic blockers, high [K+]O reduced the stimulatory effects of All, but contraction and aortic flow was still significantly greater (P < 0.01) than in high [K+]O alone. These results show that All can ameliorate the depressive effects of high [K+]O on the heart. The local release of All in the heart during activation of the sympathetic nervous system and the rise in circulating All during exercise could therefore play a role in protecting the heart from hyperkalaemia.
儿茶酚胺可恢复因高钾血症（升高的[K⁺]O）和酸中毒而受抑制的心脏收缩，然而在运动过程中，高钾血症和酸中毒在β肾上腺素能阻滞剂作用下仍可被耐受。为了测试升高的[K⁺]O的负面影响是否被一种非肾上腺素能激素抵消，将血管紧张素II（AII）给予在37℃下用8和10 mM K⁺的台氏液灌注的兔乳头肌（AII 75 nM，n = 9）和兔离体工作心脏（AII 5 nM，n = 8）。对另外9个用普萘洛尔（1 μM）和哌唑嗪（1 μM）处理的离体心脏也进行了类似的实验方案。在正常台氏液中，所有这些处理均导致收缩和主动脉血流显著（P < 0.01）增加，并在高[K⁺]O期间维持主动脉血流。在用肾上腺素能阻滞剂处理的乳头肌和离体心脏中，高[K⁺]O降低了AII的刺激作用，但收缩和主动脉血流仍显著（P < 0.01）大于仅处于高[K⁺]O时。这些结果表明AII可改善高[K⁺]O对心脏的抑制作用。因此，交感神经系统激活期间心脏中AII的局部释放以及运动期间循环中AII的升高可能在保护心脏免受高钾血症影响方面发挥作用。
