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Acute alcohol withdrawal increases sodium transporter expression in rat kidneys
Muhammad Syed1, Zaria Opara1, Jelani Thompson1
1Department of Physiology and Biophysics, Howard University College of Medicine, Washington DC, 20059, USA.
Alcohol (Fayetteville, N.Y.)
|February 13, 2026
Summary
Alcohol withdrawal alters kidney protein expression, increasing sodium transporters (NCC, NKA, NCX1) and decreasing water channel Aqp2. These changes may contribute to alcohol-related kidney dysfunction.
Area of Science:
- Nephrology
- Alcoholic research
- Molecular biology
Background:
- Alcohol consumption impacts blood pressure, electrolyte, and water balance, with kidneys playing a crucial role.
- Renal mechanisms during alcohol consumption and withdrawal are not fully understood.
Purpose of the Study:
- Investigate changes in key renal proteins during acute alcohol withdrawal.
- Analyze expression of sodium chloride cotransporter (NCC), Na-K-ATPase (NKA), sodium-calcium exchanger (NCX1), and Aquaporin-2 (Aqp2).
Main Methods:
- Adult male and female Sprague-Dawley rats received alcohol for 4 days, followed by 24 or 48 h withdrawal.
- Western blotting determined protein expression in renal cortical membranes.
- Control groups received a vehicle without alcohol.
Main Results:
- Alcohol withdrawal increased NCC expression in both sexes at 24 and 48 h.
- NKA expression increased in males at 24 h but not females.
- NCX1 expression transiently increased in females at 24 h.
- Aqp2 expression decreased in both sexes post-withdrawal.
Conclusions:
- Alcohol withdrawal alters renal protein expression, upregulating NCC, NKA, and NCX1.
- Downregulation of Aqp2 during withdrawal suggests impaired water balance.
- These molecular changes may underlie alcohol-induced kidney dysfunction.
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