Korean J Nephrol.  2009 Jan;28(1):1-9.

Pathophysiological Implications of Sodium Transporters and Water Channels in the Kidney

• Kim SW
• Ma SK
• Bae EH
• Park JW
• Lee JU

Abstract

Renal sodium and water reabsorption occurs through epithelial sodium transporters and aquaporin (AQP) water channels in various segments of tubules. We have demonstrated altered regulation of these transporters and channels in various pathophysiological conditions. In nephrotic syndrome and liver cirrhosis, expression of epithelial sodium channels (ENaC) was increased in the late distal convoluted tubule, connecting tubule, and collecting duct. In spontaneously hypertensive rats, the expression of Na,K-ATPase as well as that of ENaC was increased. In contrast, AQP1-3 and sodium transporters was decreased in the kidney from deoxycorticosterone acetate-salt hypertension. In two-kidney, one clip hypertension, the expression of Na,K-ATPase, NHE3, NKCC2 and ENaC subunits was decreased in the clipped kidney while remained unchanged in the contralateral kidney. We have also shown an increased activity of renal atrial natriuretic peptide system in postobstructive natriuresis/ diuresis. In acute kidney injury (cisplatin-, gentamicin- and ischemia/reperfusion-induced), the expression of Na,K-ATPase, NHE3, NKCC2 and AQP1-3 was decreased. The altered regulation of sodium transporters and AQP may be causally related with various kidney diseases and hypertension.

MeSH Terms

Acute Kidney Injury
Aquaporins
Desoxycorticosterone
Diuresis
Epithelial Sodium Channels
Hypertension
Kidney
Kidney Diseases
Liver Cirrhosis
Nephrotic Syndrome
Rats, Inbred SHR
Sodium
Aquaporins
Desoxycorticosterone
Epithelial Sodium Channels
Sodium