Abstract
Larval Ambystoma tigrinum (59-199 g) were treated with the drug aminoglutethimide (6 mg/day) in order to abolish steroid hormone synthesis. Steroid deprivation prevented the increase in plasma aldosterone concentration observed in sham-infused larvae during respiratory acidosis. It also blocked the normal compensatory response to respiratory acidosis of elevated plasma [HCO3-] and inhibited cutaneous Na+ transport. Aldosterone (10 μg/day) and, to a lesser extent, corticosterone (240 μg/day) restored the compensatory response. Aldosterone replacement also stimulated cutaneous Na+ transport in AG-inhibited larvae. The results suggest that aldosterone, at about 1000 pg/ml, supports the compensatory ionic responses to respiratory acidosis in this species.
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