Renal structural and functional changes and sodium balance in hypothyroid rats.

Li Bok Nam, F Fekete, L Hársing
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Abstract

Significant retardation in body and kidney growth and in renal glomerular and proximal tubular development was observed in hypothyroid rats in comparison with euthyroid controls. Body mass was found to increase by 40% but kidney mass only by 3.5% over a period of 3 weeks following thyroidectomy in contrast to an average increment of 178 and 113%, respectively, in normal animals. Dissociation was found also in the development of glomeruli and proximal tubules: glomerular size correlated with body weight while tubular size with kidney weight. Single nephron glomerular filtration rate was adapted not to the glomerular as normally but rather to the tubular volume thereby compensating functionally for the dimensional glomerulotubular imbalance. However, despite the decreased filtered and excreted amount of sodium relative to the body weight sodium balance was maintained by depressed tubular reabsorption which was uniformly observed in thyroid deficiency. Because of the uncertainty regarding the direct action of thyroid hormones on the tubular function it is assumed that decreased tubular sodium reabsorption is principally caused by the mechanism subserving the maintenance of sodium balance also in salt loaded normal and sodium sensitive Dahl's rats. This seems to be supported by the exaggerated natriuresis observed both in hypothyroid and sodium sensitive Dahl's rats after saline infusion. Justification of the proposed mechanism needs further investigation.

甲状腺功能减退大鼠肾脏结构、功能改变及钠平衡。
与甲状腺功能正常的大鼠相比,甲状腺功能减退大鼠的身体和肾脏生长以及肾小球和近端肾小管发育明显迟缓。在甲状腺切除术后的3周内,体重增加了40%,但肾脏重量仅增加了3.5%,而正常动物的平均增加量分别为178和113%。在肾小球和近端小管的发育中也发现了分离:肾小球大小与体重相关,而小管大小与肾脏重量相关。单肾元肾小球滤过率不像正常情况那样适应肾小球,而是适应肾小管体积,从而在功能上补偿了肾小管尺寸失衡。然而,尽管滤过和排泄的钠相对于体重减少,但钠的平衡是通过抑制小管重吸收来维持的,这在甲状腺缺乏症中是一致的。由于甲状腺激素对肾小管功能的直接作用尚不确定,我们认为肾小管钠重吸收的减少主要是由维持钠平衡的机制引起的,在正常和钠敏感的达尔氏大鼠中也是如此。在甲状腺功能减退和钠敏感的达尔氏大鼠中观察到的盐水输注后的过度尿钠似乎支持了这一点。拟议机制的合理性需要进一步调查。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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