Kawata H
Jpn J Physiol. 1978;28(5):709-20. doi: 10.2170/jjphysiol.28.709.
Effects of hypertonic urea solution on potassium contracture were investigated in a bullfrot ventricular strip. In a medium of three times hypertonic urea, the contracture induced by 100 mM potassium solution was markedly inhibited whereas the twitch contraction was augmented in the hypertonic urea solution. The extent, as well as the time course, of the membrane depolarization produced by high potassium solution was essentially identical in both isotonic and hypertonic conditions. Endogeneous catecholamine does not seem to participate in this inhibition since the treatment with propranolol did not modify the results. Thus, the possibility of the well-known catecholamine-induced inhibition of potassium contracture can be excluded. The myocardial contractility was never suppressed, or even augmented, at this stage of urea perfusion although a prolonged hypertonic urea perfusion gradually suppressed the contractility. It was suggested that hypertonic urea exerts its negative inotropic action on the potassium contracture independently of its positive inotropism on the twitch contraction by accelerating the uptake of the activator calcium ion to some undefined intracellular sites.
在牛蛙心室肌条上研究了高渗尿素溶液对钾挛缩的影响。在三倍高渗尿素的介质中，100 mM钾溶液诱导的挛缩受到显著抑制，而在高渗尿素溶液中抽搐收缩增强。高钾溶液引起的膜去极化程度和时间进程在等渗和高渗条件下基本相同。内源性儿茶酚胺似乎不参与这种抑制作用，因为用普萘洛尔处理并没有改变结果。因此，可以排除众所周知的儿茶酚胺诱导的钾挛缩抑制作用的可能性。在尿素灌注的这个阶段，心肌收缩力从未受到抑制，甚至增强，尽管长时间的高渗尿素灌注会逐渐抑制收缩力。有人提出，高渗尿素通过加速激活钙离子向某些未明确的细胞内位点的摄取，对钾挛缩发挥其负性肌力作用，而与它对抽搐收缩的正性肌力作用无关。
