Inhibition of aldosterone-induced antinatriuresis and kaliuresis by actinomycin D.
The effects of actinomycin D on short-term response to aldosterone on sodium and potassium urinary excretion were investigated in adrenalectomized glucocorticoid-substituted anesthetized rats. Aldosterone alone (1 microgram/kg followed by sustained intravenous infusion of 1 microgram X kg-1 X h-1) entailed a simultaneous antinatriuretic and kaliuretic effect after a latent period of 30-60 min. Actinomycin D (300 micrograms/kg) administered intravenously 30 min before aldosterone inhibited both the aldosterone-induced kaliuresis and antinatriuresis and the concomitant changes in plasma potassium concentration. The administration of actinomycin D alone enhanced sodium excretion in the first hour and then induced kaliuresis. These results favor the hypothesis that mineralocorticoid effects of aldosterone on sodium and potassium excretion are closely linked and may be dependent on the same mechanisms.
D000315:Adrenalectomy; D000450:Aldosterone / Q000494:pharmacology*; D000818:Animals; D003609:Dactinomycin / Q000494:pharmacology*; D008297:Male; D000451:Mineralocorticoid Receptor Antagonists / Q000494:pharmacology; D009318:Natriuresis / Q000187:drug effects*; D011188:Potassium / Q000652:urine*; D051381:Rats; D011919:Rats, Inbred Strains
D000451:Mineralocorticoid Receptor Antagonists; D003609:Dactinomycin; D000450:Aldosterone; D011188:Potassium