Interrenal function in larval Ambystoma tigrinum. II. Control of aldosterone secretion and electrolyte balance by ACTH.
Renal clearance techniques were used to assess the role of ACTH on renal electrolyte transport in larval Ambystoma tigrinum. Radioimmunoassay was employed to evaluate changes in circulating aldosterone in these animals. Larvae were hypophysectomized and maintained for 1 week on either ACTH replacement therapy (50 ng/g) or sham injections prior to clearance measurements. Hypophysectomy significantly lowered plasma [Na+] (from 96 to 90 mM), plasma [K+] (from 6 to 4 mM), plasma aldosterone titer (from 157 to 36 pg/ml), fractional Na+ reabsorption (from 97 to 94%), and fractional K+ reabsorption (from 68 to 50%). ACTH replacement restored plasma [Na+] to 96 mM, aldosterone titer to 157 pg/ml, fractional Na+ reabsorption to 96%, and fractional K+ reabsorption to 75%. When steroid synthesis was blocked in a separate set of larvae; ACTH was unable to reverse the sodium depletion which results from adaptation to distilled water. This suggests that ACTH is not acting directly on Na+ transport but acts through a steroid like aldosterone. When larvae were injected intravenously with antialdosterone antibodies their fractional Na+ reabsorption decreased from 95 to 87%. We conclude, therefore, the ACTH works via interrenal steroids, such as aldosterone, to control renal electrolyte transport in this species.
D000324:Adrenocorticotropic Hormone / Q000494:pharmacology*; D000450:Aldosterone / Q000378:metabolism*; D000557:Ambystoma / Q000502:physiology*; D000818:Animals; D001693:Biological Transport, Active / Q000187:drug effects; D007016:Hypophysectomy; D007668:Kidney / Q000502:physiology*; D007814:Larva / Q000502:physiology; D010902:Pituitary Gland / Q000502:physiology; D011188:Potassium / Q000378:metabolism; D012964:Sodium / Q000378:metabolism; D014882:Water-Electrolyte Balance / Q000187:drug effects
D000450:Aldosterone; D000324:Adrenocorticotropic Hormone; D012964:Sodium; D011188:Potassium