Segments of the Nephron Flashcards
Renal corpuscle
Contains glomerulus and Bowman’s capsule
Rapid ultrafiltration from blood capillary of glomerulus into Bowman’s space (or, urinary space). Pretty much everything but proteins (albumin) and RBCs gets through.
Urinary pole leads to PCT, vascular pole has afferent/efferent arterioles
Proximal convoluted tubule
Reabsorbs 65-70% of filtrate
Isosmotic reabsorption (water and solute absorbed has same osmolality as filtrate)
Glucose, AAs, some organic acids 100% absorbed
Other organic acids/bases 100% secreted
Urea 50% reabsorbed passively
Early PCT reabsorbs NaHCO3 and late PCT reabsorbs NaCl
NH4+ secreted here, that eventually helps excrete H+ if you get acidosis
Has glomerulotubular balance (if GFR increases reabsorption increases)
Thin descending limb of loop of Henle
Passively permeable to water and small solutes (NaCl, urea)
Water moves out and solutes move in and tubular fluid becomes more concentrated (hyperosmotic) as it flows down
Thin, flat epithelia and no mitochondria
Contributes to countercurrent multiplier
Thin ascending limb of loop of Henle
Not permeable to water, but is passively permeable to NaCl
Solute moves out (without water) so tubular fluid becomes less concentrated (hyposmotic) as it flows up
Thin, flat epithelia and no mitochondria
Contributes to countercurrent multiplier
Thick ascending limb of loop of Henle
Reabsorbs 25% of filtered solute but impermeable to water
Highest Na/K ATPase activity in the kidney (basolateral membrane)
Is load dependent (the more Na+ delivered, the more it will reabsorb)
Dilutes urine
Contains macula densa cells
Sets up countercurrent mutiplier
Has glomerulotubular balance
Juxtaglomerular apparatus (JGA)
Macula densa in the thick ascending limb of loop of Henle touch the glomerulus and the juxtaglomerular cells of the afferent arteriole
When renal arterial pressure, Na+ delivery to distal tubule decrease (or when sympathetic tone increases), macula densa cells sense Na+ decrease and tell JG cells to secrete renin, which activates RAAS system to increase water reabsorption, increase BP, increase GFR, etc
Distal convoluted tubule
Reabsorbs 5% of filtered solute but not much water
Dilutes urine further
Similar to thick ascending limb of loop of Henle, but different transport mechanisms
Hormonal regulation of Ca2+ reabsoprtion
Has GT balance
Collecting tubule
Principal cells: most common type (65%); regulate K+, Na+, H2O; acted on by aldosterone and ADH; dilute/concentrate the urine
Type I (alpha) intercalated cells: secrete H+ and reabsorb K+
Establishes steep gradient, but have limited capacity (quality control at the end of long assembly line)
Early proximal convoluted tubule reabsorption of Na+
Apical membrane:
1) Na+ channels
2) Na+ cotransporters w/glucose, AAs, phosphate
3) Na/H antiport (MOST IMPORTANT)
Basolateral membrane: Na/K ATPase pumps Na+ into plasma against gradient
Lumen is -4mV because of Na+ reabsorption
Remember, HCO3- reabsorbed with Na+ (electroneutrality!) from CO2 inside the cell
Late proximal convoluted tubule reabsorption of Na+
1/3 of Na+ and water have already been reabsorbed but [Na+] still the same!
Not much glucose, AAs, etc left for cotransport with Na+
BUT, Cl- concentration in lumen is increased 20% compared to plasma concentration so there is steep electrochemical gradient for its passive reabsorption. Lumen at +4mV because of Cl- moving into cell in early PCT, but CHEMICAL gradient forces Cl- into cell anyway, and Cl- brings Na+ with it (electroneutrality):
1) NaCl through leaky-ish tight junctions (30% of reabsorption in PCT)
2) Cl/Formate exchange with Na/H and HF leaving cell as H+ and F- drives this
Early proximal convoluted tubule reabsorption of Cl-
Cl- not preferentially absorbed in PCT (HCO3- is), but goes through VERY leaky tight junctions because lumen is -4mV compared to cell
Water reabsorption in PCT
Standing gradient hypothesis (Jared Diamond) across lateral membranes (between cells–so much more SA than other membranes) that has isosmotic in it. Closed at lumen end but open at basolateral end, and most Na/K ATPase at basolateral end so water diffuses there! (Costanzo says it is high oncotic pressure of peritubular capillary that draws fluid in from lateral space)
With aquaporins in lateral membranes
Also water is passively reabsorbed (water follows salt) in luminal membrane and basolateral membrane
Urea reabsorption in PCT
As solute and water are reabsorbed in the PCT, a concentration gradient for urea to move into the plasma arises (more urea in PCT than in capillaries)
50% of urea diffuses down its gradient and is reabsorbed using channels, but not that permeable so only 50%.
Note: urea not reabsorbed here does not get reabsorbed again until collecting duct
Note: urea transport proteins in collecting duct inculde ADH-activated urea channels
Glomerulotubular balance
Increased GFR causes proportionate increase of reabsorption (percent of filtrate reabsorbed is constant, so if more filtrate, more reabsorbed)
How: more fluid filtered out of glomerular capillaries, leaving higher leftover protein concentration and oncotic pressure of blood that ends up in peritubular capillaries, and that causes higher reabsorption (Increase GFR –> increase filtration fraction –> increase oncotic pressure in peritubular capillaries –> increase reabsorption)
Dependent on glucose, AA, HCO3 for increased cotransport of Na+
Prevents increased GFR from overwhelming downstream transport capacity
PCT has GT balance (it’s so awesome for being able to do this!)
How is GT balance in the PCT affected by volume state?
Hypervolemia: increased ECF volume –> increased extracellular water dilutes plasma proteins –> decreased oncotic pressure in capillaries but increased hydrostatic pressure –> increased hydrostatic pressure of interstitial fluid around PCT –> increased leakiness of tight junctions –> Na+ goes back into lumen through tight junctions and brings water with it –> decreased reabsorption of Na+ and water –> more Na+ and water excreted, and get rid of volume!
