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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.

Original publication




Journal article


Acta Physiol Scand

Publication Date





419 - 427


Angiotensin II, Animals, Dose-Response Relationship, Drug, Heart, Heart Rate, Muscle Contraction, Potassium, Rabbits