| Pathophysiological Implications of Sodium Transporters and Water Channels in the Kidney |
| Soo Wan Kim, M.D.1, Seong Kwon Ma, M.D.1, Eun Hui Bae, M.D.1, Jeong Woo Park, M.D.1 and Jong Un Lee, M.D.2 |
| Departments of Internal Medicine1 and Physiology2 Chonnam National University Medical School, Gwangju, Korea |
| 추모논문 : 신장에서 나트륨 수송체와 수분 통로의 병태생리 |
| 김수완1, 마성권1, 배은희1, 박정우1, 이종은2 |
| 전남대학교 의과대학 내과학교실1, 생리학교실2 |
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| Abstract |
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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. |
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