Hormonal effects on Na-K-ATPase of various parts of the rat nephron.
Aldosterone reactivates the impaired Na-K-ATPase very rapidly along the course of the distal tubule and in the proximal convolution. Surprisingly the latent period before enzyme induction parallels with the latent period before the restoration of active sodium reabsorption after a physiological dose of aldosterone [7]. Induction of Na-K-ATPase can be prevented by cycloheximide or actinomycin D, inhibitors of protein synthesis; this proves that protein synthesis is necessary for the induction of Na-K-ATPase. Although this kind of data can be interpreted as due to de-novo-synthesis for the induced enzyme this conclusion is not proved by such data. Another way of aldosterone action could exist in demasking inactive enzyme molecules which are already present in the membrane. Because of the very short latent period between aldosterone application and restoration of Na-K-ATPase we cannot exclude this possibility. The most important finding of our study is the rapid reactivation of the impaired Na-K-ATPase in the proximal and distal tubule after a single dose of aldosterone.
D000251:Adenosine Triphosphatases / Q000378:metabolism*; D000315:Adrenalectomy; D000450:Aldosterone / Q000494:pharmacology*; D000818:Animals; D003513:Cycloheximide / Q000494:pharmacology; D003609:Dactinomycin / Q000494:pharmacology; D007668:Kidney / Q000201:enzymology*; D007684:Kidney Tubules / Q000201:enzymology; D008297:Male; D009399:Nephrons / Q000201:enzymology*; D011188:Potassium / Q000494:pharmacology; D051381:Rats; D012964:Sodium / Q000494:pharmacology
D003609:Dactinomycin; D000450:Aldosterone; D003513:Cycloheximide; D012964:Sodium; D000251:Adenosine Triphosphatases; D011188:Potassium