The effects of aldosterone on sodium and potassium metabolism in larval Ambystoma tigrinum.
Electrolyte depletion resulting from 14 days in distilled water, which was changed daily, lowered plasma Na concentration from 108 to 92 mM. Aminoglutethimide was administered on each of the final 3 days of the depletion period in doses of 3 mg/animal. This further depressed Na to 75 mM. Both aldosterone (25 micrograms/animal) and corticosterone (200 micrograms/animal) returned plasma Na to 92 mM. Cortisone (200 micrograms/animal) was ineffective. There were no consistent patterns in plasma K. Renal clearance experiments showed that the same dose of aminoglutethimide decreased fractional tubular Na reabsorption and increased fractional tubular K reabsorption. Aldosterone reversed these trends suggesting that this hormone may play a role in controlling renal electrolyte excretion.
D000450:Aldosterone / Q000494:pharmacology*; D000557:Ambystoma / Q000378:metabolism*; D000616:Aminoglutethimide / Q000494:pharmacology; D000818:Animals; D003345:Corticosterone / Q000494:pharmacology; D000431:Ethanol / Q000494:pharmacology; D007684:Kidney Tubules / Q000187:drug effects / Q000378:metabolism; D007814:Larva / Q000378:metabolism; D011188:Potassium / Q000378:metabolism*; D012964:Sodium / Q000172:deficiency / Q000378:metabolism*
D000616:Aminoglutethimide; D000431:Ethanol; D000450:Aldosterone; D012964:Sodium; D011188:Potassium; D003345:Corticosterone