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Aldosterone-induced glycoproteins: electrophysiological-biochemical correlation
H M Szerlip1, L Weisberg, K Geering
1Renal-Electrolyte Section, Veterans Administration Medical Center, Philadelphia, PA 19104.
Biochimica Et Biophysica Acta
|May 9, 1988
Summary
Aldosterone stimulates toad bladder glycoprotein synthesis (GP65,70) during a late phase of its natriferic action. These glycoproteins are not the beta subunit of the sodium-potassium pump (Na+/K+-ATPase).
Area of Science:
- Endocrinology
- Molecular Biology
- Physiology
Background:
- Aldosterone is a hormone that regulates sodium transport.
- Aldosterone induces synthesis of glycoproteins (GP65,70) in toad bladders.
- These glycoproteins are potential effectors of aldosterone's natriferic action.
Purpose of the Study:
- To investigate the synthesis and function of GP65,70 in response to aldosterone.
- To determine if GP65,70 is the beta subunit of Na+/K+-ATPase.
Main Methods:
- Two-phase electrophysiological response analysis of aldosterone.
- Biosynthetic labeling of toad bladders with [35S]methionine.
- Biochemical analysis of GP65,70 and amphibian renal beta subunit.
Main Results:
- Aldosterone induced a two-phase electrophysiological response: early (conductance increase) and late (current increase).
- GP65,70 synthesis occurred during the late phase of aldosterone action.
- GP65,70 was biochemically similar but immunologically distinct from the beta subunit of Na+/K+-ATPase.
Conclusions:
- GP65,70 is synthesized as a late effect of aldosterone in toad urinary bladders.
- GP65,70 is not the beta subunit of Na+/K+-ATPase.
- The precise cellular function of GP65,70 remains to be determined.