Renal sodium reabsorption
Renal reabsorption of sodium (Na+) is a part of renal physiology. It uses Na-H antiport, Na-glucose symport, sodium ion channels (minor). It is stimulated by angiotensin II and aldosterone, and inhibited by atrial natriuretic peptide.
Most of the reabsorption (65%) occurs in the proximal tubule. In the latter part it is favoured by an electrochemical driving force, but initially it needs the cotransporter SGLT and the Na-H antiporter. Sodium passes along an electrochemical gradient (passive transport) from the lumen into the tubular cell, together with water and chloride which also diffuse passively. Water is reabsorbed to the same degree, resulting in the concentration in the end of the proximal tubule being the same as in the beginning. In other words, the reabsorption in the proximal tubule is isosmotic.
Loop of Henle
Sodium is reabsorbed in the thick ascending limb of loop of Henle, by Na-K-2Cl symporter and Na-H antiporter. It goes against its chemical driving force, but the high electrical driving force renders the overall electrochemical driving force positive anyway, availing some sodium to diffuse passively either the transcellular or paracellular way.
Although only a fragment of total reabsorption happens here, it is the main part of intervention. This is e.g. done by endogenous production of aldosterone, increasing reabsorption. Since the normal excretion rate of sodium is ~100mmoles/day, then a regulation of the absorption of still more than 1000 mmoles/day entering the collecting duct system has a substantial influence of the total sodium excreted.
|Characteristic||proximal tubule||loop of Henle||Distal convoluted tubule||Collecting duct system|
|S1||S2||S3||descending limb||thin ascending limb||thick ascending limb||connecting tubule||initial collecting tubule||cortical collecting ducts||medullary collecting ducts|
|electrical driving force (mV)||-3||+3||+15||-5 to +5||-40|
|chemical driving force (mV)||0||0||-9||-19||-34|
|electrochemical driving force (mV)||-3||+3||+6||-24 to -14||-74|
|apical transport proteins||SGLT, Na-H antiporter||(passively)||Na-K-2Cl symporter
(Na-H antiporter and passively)
|basolateral transport proteins||Na+/K+-ATPase|
|Other reabsorption features||isosmotic||by principal cells, stimulated by aldosterone|
- VI. Mechanisms of Salt & Water Reabsorption
- Walter F., PhD. Boron. Medical Physiology: A Cellular And Molecular Approaoch. Elsevier/Saunders. ISBN 1-4160-2328-3. Page 776
- Walter F., PhD. Boron. Medical Physiology: A Cellular And Molecular Approaoch. Elsevier/Saunders. ISBN 1-4160-2328-3. Page 777
- Walter F., PhD. Boron. Medical Physiology: A Cellular And Molecular Approaoch. Elsevier/Saunders. ISBN 1-4160-2328-3. Page 778