Transport Processes I: Na, Cl HCO3, H20, Sugar and AA transport Flashcards
(25 cards)
What are the most important electrochemical and concentration gradients to remember for any cell?
-Na concentration is low inside cells
-K concentration is high inside cells
Resting membrane potential:
-inside neg relative to outside
-because potassium flows out passively when K channels are open
Transport in the proximal tubule: characteristics
- 2/3 of Na, Cl and H20 are reabsorbed here (he said remember this!)
- Reabsorption is isoosmotic (H20 follows the flow of solutes)
- the Na/K ATPase is the primary driving force for transport
How is sodium reabsorbed in the first half of the PT?
Sodium reabsorbed via Na/H antiporter
- This is coupled to HC03 reabsorption (memb bound and intracellular CA)
- HC03 crosses basolateral memb. via Cl/HC03 exchanger and Na/HC03 cotransporter
How are sugars and amino acids reabsorbed in the first half of the PT?
Sugars/AAs are coupled to Na transport via Na-coupled cotransporters
-driven by the low cytoplasmic Na concentration
Sugars cross basolateral memb. via passive transporters
How is sodium reabsorbed in the second half of the PT?
- Na reabsorbed via Na/H antiporter
- H+ reenters from lumen by combining with anions
- anions recycled back into the lumen via Cl- exchanger which allows for Cl- reabsorption (no Cl- reabsorption in first half of PT)
Paracellular transport in the PT
- what creates the transepithelial potential?
- what is transported this way?
- Remember that lumenal CL- conc. increases in the first half of the PT because it isn’t reabsorbed there
- this creates an osmotic gradient driving Cl- reabsorption from lumen into interstitium via paracellular transport
- Cl- paracellular transport creates a transepithelial memb potential (lumenal positive) which will drive Na and K reabsorption into the interstitium via paracellular transport.
What happens in the thin descending limb of the loop?
It is permeable to water. The concentration increases as the TDL descends into the medulla, driving more and more water reabsorption.
What about the thin ascending limb of the loop?
It is impermeable to water. But permeable to Na and Cl- so they are reabsorbed passively as the thin ascending limb ascends, but water cant follow
Na and Cl- transcellular transport in the thick ascending limb of the loop
- Na, K and Cl taken up together via Na/K/2Cl co-transporter
- Na also reabsorbed by Na/H antiporter
paracellular transport in the thick ascending limb of the loop of henle
- thick ascending limb has apical K+ channels
- K+ exit into lumen through these creates lumenal positive transepithelial potential that drives paracellular uptake of cations (Na, Ca, K and Mg)
- But no “solvent drag” cuz thick ascending limb of loop impermeable to H20
What does furosemide do?
-inhibits the Na/K/2Cl co-transporter in the thick ascending limb of the loop
What is Barterr’s syndrome?
-Genetic defect resulting in defective Na/K/2Cl co-transporter in the thick ascending limb of the loop
-characterized by hypokalemia
“Bartering is a loop”
What controls water reabsorption in the Distal Tubule and Collecting Duct?
-ADH
high ADH: increased H20 permeability, concentrated urine
low ADH: decreased H20 permeability, dilute urine
Na and Cl reabsorption in early part of DT
- Early DT impermeable to H20
- Na and Cl- reabsorbed via Na/Cl cotransporter
- Cl crosses basolateral membrane via Cl- channels
What does thiazide do?
-inhibits the Na/Cl cotransporter in the early part of the DT
What is Gitelmans syndrome?
- defective Na/Cl cotransporter in early part of DT
- hypotension
- hypokalemia
What are the two types of cells in the late DT and collecting duct?
(how to remember which is which)
- Principal Cells: absorb Na+ via apical Na+ channels
- “Principal cells absorb the principal ion”
- alpha-intercalated cells secrete H+ into the lumen of the Renal tubule
- In Chemistry, intercalation is the insertion of a molecule or ion into compounds with layered structures: “intercalated cells are inserting H+ into the lumen of the RT”
Whats going on in the principal cells of the late DT and collecting duct?
principal cells have:
- apical Na+ channels (Na flows in passively)
- apical K+ channels (K flows out passively)
- and they are permeable to H20 (controlled by ADH)
Describe paracellular transport in the late DT and collecting duct.
- the transepithelial membrane potential is lumenal negative here
- Therefore Cl- reabsorption can occur paracellularly
What does Amiloride do?
-inhibit the apical Na+ channel in principal cells
What is Liddle’s Syndrome?
-mutation in the apical Na channel of principal cells
-it is a GAIN OF FUNCTION mutation (rare)
-so it results in increased sodium reabsorption, resulting in hypertension
“Liddle’s is a defect in a ‘Liddle’ transporter: the apical Na channel”
What causes diabetes Insipidus?
The H20 permeable channels in principal cells become insensitive to ADH
What happens in the intercalated cells of the late DT and collecting duct?
- alpha intercalated cells contain an apical proton pump (V-ATPase that pumps H+ into the RT lumen
- also contain a basolateral Cl-/HC03- exchanger that allows HC03- exit into the blood (gotta balance with H+ secretion)
What causes renal tubule acidosis?
-Genetic defects in the renal specific isoforms of V-ATPase
