Cardiovascular Research Institute and the Department of Medicine, University of California School of Medicine, San Francisco.
J Gen Physiol. 1963 Mar 1;46(4):733-54. doi: 10.1085/jgp.46.4.733.
The relationship of the short-circuit current to metabolism was studied in the toad bladder in vitro. Substrates and inhibitors were added to the bathing medium and the effect on the short-circuit current was determined. The spontaneous decline in the short-circuit current that occurred in substrate-free media was prevented or reversed by the addition of glucose, pyruvate, lactate, or beta-hydroxybutyrate, whereas acetate and tricarboxylic acid cycle intermediates had no effect. A variety of metabolic inhibitors depressed the short-circuit current; depression by iodoacetate and by malonate was delayed by prior addition of pyruvate or lactate but not by glucose. The ability of a substrate to stimulate the current did not correlate with its rate of oxidation to CO(2). On the basis of earlier studies, the metabolic effects on the short-circuit current were assumed to reflect equivalent effects on the rate of active Na transport. It is suggested that the energy for Na transport is provided not by a general cellular metabolic pool but by a specific metabolic pathway or pathways spatially linked to the transport mechanism.
本研究旨在探讨体外蟾蜍膀胱短电流与代谢的关系。向灌流液中加入底物和抑制剂，测定其对短电流的影响。无底物灌流液中自发出现的短电流下降可被葡萄糖、丙酮酸盐、乳酸或β-羟丁酸所阻止或逆转，而乙酸盐和三羧酸循环中间产物则无此作用。多种代谢抑制剂均可抑制短电流；碘乙酸盐和丙二酸盐的抑制作用可被丙酮酸盐或乳酸盐预先加入所延迟，但葡萄糖无此作用。底物刺激电流的能力与其氧化生成 CO2 的速率无关。根据先前的研究，短电流的代谢效应被假定反映了对主动 Na 转运速率的等效影响。因此，Na 转运的能量不是由一般的细胞代谢池提供，而是由与转运机制空间相关的特定代谢途径或途径提供。
