Renal Transport Flashcards
different transport mechanisms by energy source
Passive: down EC gradient
- simply or facilitated (pores, channels, carrier proteins) diffusion
active transport: against EC gradient, requires E
- primary= using ATP hydrolysis
- secondary=coupling transport up EC gradient with transport down EC gradient
unique properties of epithelial cells, how these influence transport along nephron
- polar (distinct apical and basolateral)
- tight junctions near apical surface segregate membrane surfaces, determine transport directionality
- electric potential diff across peritubular space (0mV) and lumen with can be -, +, or 0
- apical SA amplified by brush border
major pathways of Na+ transport along nephron, how distribution of tranposrters (apical/basal) allow regulation of transport
BULK Na+ reabsorption in PT
Regulation of Na+ reabsorption in CD
transport depends on:
- available transporters
- regional permeability
- composition delivered tubular fluid
- transepithelial voltage gradient
proximal tubule Na+ reabsorption
Na+ reabsorption coupled with HCO3- reclamation
Na/K ATPase establish gradient
NHE3-Na/H exchanger- initiates Na+ reabsorption, secretes H+ into tubular lumen
NBC1-Na/HCO3- completes Na+ reabsorption, reclaims intracellularly produced HCO3-
OR coupled wo other solutes (glucose, a.a.)
proximal tubule H2O/Cl reabsorption
Na+ reabs. promotes this.
bulk H2O movement will pull Cl- across tight junctions (solvent drag)
transepithelial EC gradient promotes paracellular CL- transport
transcellular Cl- transport path: apical and basolateral transporter
thick ascending limb Na+ reabsorption
ascending thin limb = some passive Na_ reabsorption
TAL: NCC2 and Na/K ATPase
- generates hypertonic interstitium, hypotonic tubular fluid that re-enters cortex in DCT
- K+ recycled to tubular lumen, creates lumen-positive
which promotes paracellular cation reabsorption
distal tubule Na+ reabsorption
principal cells of DCT
first portion relies on NCC
second relies on NCC and ENaC
CD Na+ reabsorption
principal cells of CD rely on ENaC
site of regulation. tuned by aldosterone
aldosterone enhances ENaC synthesis, and insertion of ENaC apical, and open probability
K+ Reabsorption/secretion basics
BULK reabsorption occurs in PT (same for all K+ levels)
Regulation K+ reabsorption/secretion occurs in CD
normal/elevated levels = secretion predominates
low levels=reabsorption
PT K+ reabsorption
two paths:
- solvent drag k+ reabsorption (early PT)
- active Na+ reabsorption drives H2O reabsorption, coupled with K+ - paracellular diffusion (late PT)
- positive lumen drives
composition of tubular fluid along PT
changes markedly.
- glucose/a.a./HCO3- largely reabsorbed
- amount H2O reduced (know this bc amount inulin is constant, but [] increases)
- H2O follows Na+ movement
also, transepithelial potential is negative at beginning, then becomes positive
flow rate decreases progressively, due to loss H2O
TAL K+ reabsorption
2 paths:
- transcellular K+ reabsorption
- Na/K ATPase provides gradient for NKCC2
- basolateral KCC and K+ channels - paracellular diffusion
- some K+ needs to be recycled to tubular lumen, creates lumen-positive voltage, drives diffusion
DCT K+ Secretion
KCC located apically = major pathway
couples basolateral NA/K ATPase activity to apical K+ transport
DCT late secretion relies on apical KCC and ROMK
CD K+ handling, normal/elevated VS low levels K+
normal/elevated: similar to DCT late, relies on apical KCC and ROMK in principal cells
low levels: K+ reabsorption in CD alpha-intercalated cells. apical H/K+ ATPase brings K+ into cell and reabsorption completed by basolateral channel.