Sodium Regulation: Distal Convoluted Tubule and Collecting Duct

This lesson explores how the sodium is regulated along the distal convoluted tubule (DCT) and collecting duct (CD). In particular, transcellular reabsorption via the sodium chloride cotransporter (NCC) and epithelial sodium channel (ENaC), the role of a lumen-negative potential, and how genetic mutations and thiazides and amiloride affect sodium reabsorption. For help preparing for an exam on this and other topics, visit

About 5% of the filtered sodium load is reabsorbed along the distal convoluted tubule and 4% is reabsorbed along the cortical collecting duct sodium reabsorption along the distal convoluted tubule occurs trans cellularly via sodium chloride co-transporter or ncc code transporter which transports one sodium ion and one chloride ion from the lumen into the cell

This type of transport is considered electro neutral because there is no gain of a positive or negative charge once inside the cell sodium and chloride ions are transported out across the basolateral membrane by the sodium potassium atpase and chloride ion channel respectively mutations that lead to the functional loss of the ncc co-transporter are referred to as

Gittleman syndrome which results in decreased sodium reabsorption and increased natural reefs as’ this is clinically relevant because the administration of thiazide x’ produces a similar effect thuy’s ides are a class of diuretics commonly used to treat hypertension and edema they work by inhibiting ncc dependent sodium reabsorption along the distal convoluted tubule

Which can reduce systolic and diastolic blood pressure by ten and five millimeters of mercury respectively it does this by reducing the extracellular fluid volume sodium reabsorption along the cortical collecting duct occurs trans cellularly as well via epithelial sodium channels or enoch which are located in the apical membrane of principal cells neighboring beta

Intercalated cells do not reabsorb sodium rather they reabsorb chloride via the bicarbonate chloride exchanger which is referred to as pendrick we’ll talk more about that in another lesson sodium reabsorption along the cortical collecting duct varies based on the number and activity of enoch as well as the luminal sodium concentration aldosterone is by far the

Most significant regulator of enak number and activity while arginine vasopressin or avp is known to increase in activity however it’s physiological significance remains less clear as sodium is reabsorbed by enoch it creates a lumen negative potential which establishes a driving force for the secretion of positively charged ions like potassium this is important

Because like the cells in the thick ascending limb principal cells express potassium ion channels in the apical and basolateral membrane because of this anything that increases enak dependent sodium reabsorption can lead to increased potassium secretion and hypokalemia for example hyperaldosteronism which is the excess release of aldosterone from the adrenal

Cortex leads to increased sodium reabsorption and hypokalemia likewise little syndrome which are mutations that lead to increase in act number lead to increased sodium reabsorption and hypokalemia also the use of diuretics like acetazolamide furosemide and thiazide lead to increased sodium delivery along the collecting duct the increase in luminal sodium leads to

Increased enoch dependent sodium reabsorption and hypokalemia this is one of the reasons why potassium supplements are administered in conjunction with these diuretics and why they are also referred to as non potassium sparing diuretics conversely diuretics that specifically inhibit enoch are referred to as potassium sparing diuretics inhibition of enoch not only

Decreases sodium reabsorption it decreases the driving force for potassium secretion as well amiloride and sparano lactone are two types of potassium sparing diuretics amiloride blocks inna act by occupying the channel poor while spironolactone blocks the effects of aldosterone by blocking aldosterone from binding it’s nuclear receptor which leads to a reduction

In in act number and activity in summary sodium is reabsorbed trans cellularly along the distal convoluted tubule by sodium chloride or ncc code transporters the ncc code transporter is inhibited by thigh sites sodium is reabsorbed trans cellularly along the cortical collecting duct by principle cells via the epithelial sodium channel or enoch enact dependent

Sodium reabsorption creates a lumen negative potential which promotes potassium secretion aldosterone increases enak dependent sodium reabsorption by increasing the number and activity of enoch and excessive enoch dependent sodium reabsorption can lead to hypokalemia

Transcribed from video
Sodium Regulation: Distal Convoluted Tubule and Collecting Duct By Lance Miller PhD