Loop of Henle Flashcards
What parts of the loop of Henle are relatively impermeable to water? What does the TAL help reabsorb and what percent of it is reabsorbed? What does this do to tubular fluid osmolarity? What is being done to the tubular fluid?
Thin ascending limb and thick ascending limb; Na, 25%; Decreases tubular fluid osmolarity below 100 mOsm; dilution, because you’re reabsorbing Na and Cl without taking in water
What helps create a solute concentration gradient in the nephron? Why is one of these processes particularly helpful? How does osmolarity change from cortex to inner medulla? What values can be achieved in the inner medulla?
Reabsorption of Na and Cl (active) in thick ascending limb and urea recycling in inner medulla; Defend against plasma volume depletion (dehydration) and hyperosmolarity; increases; 600-1200 mOsm/L, or 2-4 fold plasma osmolarity
What two things is reabsorptive solute transport in the TAL important for? What secretes ADH and when is it secreted? What does ADH allow for? What is no ADH is present?
- dilute tubular fluid osm to less than plasma 2. concentrating tubular fluid osmolarity in collecting duct by driving reabsorption of water from CD to circulation; posterior pituitary, in times of increased osmolarity; increase water perm of collecting duct to permit water reabsorption back into cicrulation; no water reabsorption, and tubular fluid does not equilibrate with interstitium and peritubular vasculature
What can be inserted in the collecting duct to allow for water reabsorption?
Aquaporin channels on the luminal and basolateral membranes
What three things have osmolarity less than plasma? Are they permeable to water? When is the gradient of osmolarity present from cortex to medulla? What is the controlling variable for determining if urine is dilute or concentrated? When is more water reabsorbed?
tALH, TAL, distal convoluted; No, even with ADH present; all the time; ADH levels; More water reabsorbed in times of volume contraction/hyperosmotic and you have more circulating ADH
Of the thin descending, ascending, and thick ascending, which is water permeable? How is the tubular fluid in the thin descending limb osmolarity wise? In thin ascending limb, what is reabsorbed (A or P)? In TAL, how is NaCl taken in, and what is generated?
Thin descending; tubular fluid is pretty concentrated with low NaCl permeability in thin descending; NaCl is reabsorbed passively; Use a Na-K-2Cl symporter, leading to a 200 mOsm difference between the interstitial fluid and the tubular fluid in thick ascending limb
In the TAL, how is NaCl taken in, along with K? How do they leave at the basolateral membrane? How else can Na enter the interstitium? Why? What allows for a lumen pos potential difference across the TAL membrane?
Na-K-2Cl symporter; use the Na-K ATPase, K channel, Cl channel; Na can enter paracellularly because of the lumen positive potential difference generated by K leaving at luminal membrane and Cl at basolateral; Cl leaving at basolateral and K at luminal
What could inhibit the Na-K-2Cl symporter?
Loop diuretics!!
Why does the osmolarity of the medullary interstitium get larger? With only a 200 mOsm difference in gradient between interstitium and tubular fluid, how can you get ultimately up to 1200 mOsm/L?
Counter current multiplication of solute concentration difference, ie active solute reabsorption of Na and Cl in TAL; Generate a cortico-medullary osmotic gradient by countercurrent multiplication or amplifying of TAL transport capacity
What are the steps of getting this high interstitial osmolarity?
- Pump/reabsorption of solute out of ascending limb into interstitium 2. Instant osmotic equilibration of interstitium with tubular fluid in descending limb 3. Shift of fluid along tubule and equilibration of descending limb and interstitium
What does ADH enable the kidney to do?
Defend against dehydration and excrete a concentrated urine, or defend against hyperhydration and excrete a dilute urine
How is urea moved around by the kidney? What does this help do gradient-wise? Why do we see huge changes in inner medullary osmolarity during antidiuresis vs diuresis?
Moved from collecting duct to interstitium to TAL (tubule to interstitium to tubule); Generate and maintain increased cortico-medullary gradient of hyperosmolarity; Depends on how much urea is in the interstitium during antidiuresis vs diuresis
What is the outer medulla interstitial osmolarity mostly due to? What is inner medulla interstitial osmolarity due to?
Mostly NaCl; 50% NaCl (600 mOsm) vs. 50% urea (600 mOsm)
How is urea recycled (3 steps)?
- Urea reabsorbed from inner medullary collecting duct into inner medullary interstitium 2. Urea secreted into tubular fluid of tDLH and tALH 3. Urea delivered to inner medullary collecting duct and reabsorbed into interstitium
In antidiuresis, what does ADH allow urea to do? What sustains the high interstitial urea concentration? In diuresis, is urea reabsorbed? What decreases in the inner medulla interstitium? What happens to the inner medullary interstitial osmolarity?
Allows for urea to be concentrated in tubular fluid and move down gradient into interstitium; its secretion into tDLH and tALH, allowing for continued recycling until ADH goes down; No; the interstitial urea concentration; inner medullary interstitial osmolarity consequently goes down
