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Corticosterone metabolism and membrane transport
S Sabatini1, A Hartsell, M Meyer
1Department of Physiology, Texas Tech University Health Sciences Center, Lubbock 79430.
Mineral and Electrolyte Metabolism
|January 1, 1993
Summary
Corticosterone metabolites impact kidney function. Some metabolites inhibit water flow and stimulate sodium transport in toad bladders, suggesting roles in mammalian kidney sodium and water regulation.
Area of Science:
- Renal Physiology
- Endocrinology
- Membrane Transport
Background:
- Mammalian kidneys metabolize steroid hormones, including corticosterone.
- Corticosterone receptors are present in the renal cortical collecting tubule.
- The biological activity of corticosterone metabolites is not fully understood.
Purpose of the Study:
- To investigate the functional effects of corticosterone metabolites on membrane transport.
- To analyze the oxidoreductase pathways involved in corticosterone metabolism.
Main Methods:
- Studied membrane transport in toad and turtle bladders using three corticosterone metabolites.
- Analyzed corticosterone metabolism pathways via oxidoreductase activity.
- Measured water flow and sodium transport in response to metabolites.
Main Results:
- In toad bladders, 20-dihydrocorticosterone inhibited maximal water flow, while corticosterone, 11-dehydrocorticosterone, and 20-dihydrocorticosterone stimulated sodium transport.
- Corticosterone was primarily metabolized to 11-dehydrocorticosterone, which was further metabolized to inactive 11-dehydro-20-dihydrocorticosterone.
- No significant effects on hydrogen ion secretion or corticosterone biotransformation were observed in turtle bladders.
Conclusions:
- Corticosterone metabolites may modulate sodium and water transport in the mammalian distal nephron.
- These metabolites are unlikely to regulate urinary acidification.
- Identified metabolic pathways in toad bladder mirror those in mammalian tissues.