Goodman D B, Allen J E, Rasmussen H
Proc Natl Acad Sci U S A. 1969 Sep;64(1):330-7. doi: 10.1073/pnas.64.1.330.
Studies to elucidate the mode of action of aldosterone have been carried out in the amphibian urinary bladder. The following previously reported hypotheses were evaluated: (1) aldosterone stimulates sodium transport by increasing the amount of sodium available to the sodium pump; (2) aldosterone enhances energy production for the sodium pump; and (3) aldosterone-stimulated sodium transport is obligatorily coupled to aerobic metabolism. In the present experiments, aldosterone potentiated the effect of vasopressin on sodium transport in the absence of aerobic metabolism or oxidative phosphorylation. This effect was not due to enhanced energy supply. Thus both hypotheses 2 and 3 appear not to be valid. In addition, aldosterone-stimulated sodium transport exhibited increased sensitivity to the specific inhibitor, ouabain, and this inhibition was readily reversed by K(+). These findings, as well as previously reported work, have led us to propose that aldosterone stimulates sodium transport by inducing a change either in the sodium pump itself, i.e., synthesis or activation, or in its environment in the serosal plasma membrane of the responsive cells.
关于阐明醛固酮作用机制的研究已在两栖动物膀胱中展开。对以下先前报道的假说进行了评估:(1)醛固酮通过增加钠泵可利用的钠量来刺激钠转运;(2)醛固酮增强钠泵的能量产生;(3)醛固酮刺激的钠转运必然与有氧代谢相关联。在当前实验中,在无氧代谢或氧化磷酸化的情况下,醛固酮增强了血管加压素对钠转运的作用。此效应并非由于能量供应增加。因此,假说2和3似乎均不成立。此外,醛固酮刺激的钠转运对特异性抑制剂哇巴因的敏感性增加,且这种抑制作用可被钾离子轻易逆转。这些发现以及先前报道的研究成果,使我们提出醛固酮通过诱导反应性细胞浆膜中钠泵本身(即合成或激活)或其环境的变化来刺激钠转运。