hi everyone welcome to bite size med where we talk about quick bite-sized concepts in medicine for study and rapid review this video is on the distal convoluted tubule and the collecting duct the kidney has millions of nephrons and each nephron has a glomerulus and a renal tubule the first part of the renal tubule is the proximal convoluted tubule which then leads into the loop of henle the distal convoluted tubule and finally the collecting duct functionally we can look at it in three parts the early distal tubule the late distal tubule and the cortical collecting duct
and the medullary collecting duct so let's start with the early dct this portion is continuous with the loop of henle so it's similar to the thick ascending limb of the loop of henle the early dct is impermeable to water and urea but is permeable to solutes so on the luminal membrane there is a sodium chloride co-transporter which brings sodium and chloride from the lumen into the cell the energy for this like the other parts of the nephron it comes from a sodium potassium atpase which is on the basal lateral membrane that pushes sodium out of
the cell creating a gradient which pulls sodium from the other end into the cell and that energy brings chloride along with it since chloride is coming against a concentration gradient it then diffuses along its gradient out of the cell five to ten percent of sodium is reabsorbed here so this is the site of action of thiazide diuretics and they reduce sodium chloride reabsorption a genetic defect of the sodium chloride channel is called kittleman syndrome which is autosomal recessive calcium diffuses down the concentration gradient and then gets pumped out by calcium atpase and the sodium calcium
counter transport into the interstitium similar to the thick ascending limb of the loop of henle the parathyroid hormone increases the sodium calcium exchange so there's more calcium reabsorption the late distal tubule and the cortical collecting duct are functionally similar that's why we consider them together they have two types of cells the principal cells and the intercalated cells the principal cells are more concerned with sodium and potassium while the intercalated cells are more with acid-base regulation the principal cells like the other parts of the nephron they have a sodium potassium atpase on the basolateral membrane so
that pushes three sodium out and brings two potassium into the cell the gradient created posts sodium from the lumen through the epithelial sodium channels the potassium that's secreted now into the cell because of the high concentration thanks to this pump once it gets inside it moves down its gradient to exit the cell and get into the tubular fluid only three to five percent of sodium gets reabsorbed here aldosterone has a receptor on the principal cells it increases the sodium potassium pump increasing potassium secretion now on to the intercalated cells there are two types type a
and type b both play a role in acid-base regulation but their functions are opposite to each other first let's look at type a the alpha-intercalated cells carbon dioxide diffuses into the cell it combines with water to form carbonic acid by carbonic anhydrase which then dissociates into bicarb and hydrogen ions the hydrogen ion gets actively pushed out of the cell into the lumen by hydrogen atpase and hydrogen potassium atpase the energy comes from atp so it's a primary active transport versus in the proximal convoluted tubule where the hydrogen secretion was a part of secondary active transport
with sodium the bicarb gets reabsorbed into the interstitium on exchange for chloride versus in the pct where bicarb was reabsorbed with sodium so they secrete hydrogen ions and reabsorb bicarb making them important in managing acidosis the type b beta cells do the opposite so the transporters are on the opposite side they reabsorb hydrogen ions and eliminate bicarb so they are important in managing alkalosis aldosterone has a receptor on the alpha intercalated cells as well so it increases the hydrogen atpase activity increasing hydrogen secretion and that increases bicarb chloride exchange the late dct and collecting duct
are virtually impermeable to water without the antidiuretic hormone adh creates water channels called aquaporins so they become permeable to water so this area is under the influence of adh which can control dilution or concentration of urine the medullary collecting ducts are the final site of processing they can do a few things they can reabsorb water under the influence of the anti-diuretic hormone as well they can secrete hydrogen ions against a gradient like the cortical tubule so acid-base balance and they have urea transporters so urea can move out of the nephron into the medullary interstitium and
that's important in the counter current multiplier to maintain medullary hypertensity and that is the distal convoluted tubule and the collecting duct make sure to check out my other videos on renal physiology if you have any questions or any other topics you'd want a bite-sized idea on let me know in the comments below i hope you found this video useful if you did give it a thumbs up and subscribe to my channel thanks for watching and i'll see you in the next one
