Pathophysiological Implications of Sodium Transporters and Water Channels in the Kidney.
- Author:
Soo Wan KIM
1
;
Seong Kwon MA
;
Eun Hui BAE
;
Jeong Woo PARK
;
Jong Un LEE
Author Information
1. Department of Internal Medicine, Chonnam National University Medical School, Gwangju, Korea. skimw@chonnam.ac.kr
- Publication Type:Original Article
- MeSH:
Acute Kidney Injury;
Aquaporins;
Desoxycorticosterone;
Diuresis;
Epithelial Sodium Channels;
Hypertension;
Kidney;
Kidney Diseases;
Liver Cirrhosis;
Nephrotic Syndrome;
Rats, Inbred SHR;
Sodium
- From:Korean Journal of Nephrology
2009;28(1):1-9
- CountryRepublic of Korea
- Language:Korean
-
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.
