Cortisolの近位尿細管におけるNa転送促進作用のActinomycin Dによる抑制について

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  • Inhibition of cortisol action on sodium reabsorption at the proximal tubule by actinomycin D
  • Cortisol キン イ ニョウ サイカン ニ オケル Na テンソウ ソクシン サヨウ ノ Actinomycin D ニ ヨル ヨクセイ ニ ツイテ

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In earlier studies of the action of cortisol on tubular sodium reabsorption, we have found that the hormone enhance sodium reabsorption along all parts of the nephrone except the proximal site of the distal tubule. Because the mechanism of the action had not been defined, the working hypothesis was presented that cortisol promote DNA-dependent RNA synthesis that yields an increased rate of protein synthesis. The newly synthesized proteins appear to be enzymes involved in the coupling of metabolism to sodium tran-sport. Thus, studies of cortisol action on sodium reabsorption at the proximal tubule and of its inhibition by actinomycin D were performed in Wister strain male rats using the modified technique of “distal blo-ckade”. By administering cortisol and actinomycin D with triamterene, chlorothiazide and ethacrynic acid dulring mannitol infusion with replacement of urinary losses, increments in sodium excretion were used to calculate sodium reabsorption in the proximal tubule (TNa). On the control experiments, TNa was 72.2±5.8 pEq/min(mean±s. e.) and on the cortisol administered group, TNa increased to 110.5±7.8 4aEq/min (P<0. 005). However, the enhancement by cortisol has been completely inhibited by actinomycin D as TNa was 75.4+4.8 μEq/min. It has been concluded that the mechanism of cortisol action is the enhanced m-RNA synthesis that yields an increased rate of protein synthesis.

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