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Research Article Free access | 10.1172/JCI113399
Department of Medicine, Brigham and Women's Hospital, Boston, Massachusetts 02115.
Find articles by Grossman, E. in: JCI | PubMed | Google Scholar
Department of Medicine, Brigham and Women's Hospital, Boston, Massachusetts 02115.
Find articles by Hebert, S. in: JCI | PubMed | Google Scholar
Published March 1, 1988 - More info
This study investigates the effect of variations in mineralocorticoid as well as cell sodium delivery and uptake on Na-K-ATPase activity in the mouse medullary thick ascending limb of Henle (mTALH). Pharmacologic doses of the mineralocorticoid deoxycorticosterone acetate (DOCA) resulted in a 28% increase of Na-K-ATPase activity. Furosemide-induced inhibition of sodium uptake by the mTALH cell also resulted in Na-K-ATPase activity reduction (45%). Sodium deprivation did not cause a clear change in enzyme activity, either at 3 d or 2 wk, likely reflecting the result of the opposing influences of decreased sodium delivery and increased endogenous aldosterone. Finally, the behavior of Na-K-ATPase activity at 3 d of sodium deprivation in the mTALH contrasted with a 60% increase in activity observed in the cortical collecting tubule, a nephron segment known to be responsive to mineralocorticoid, and this heterogeneity of response may suggest an important role for the mTALH in maintaining salt homeostasis.