Renal Transport Flashcards

1
Q

different transport mechanisms by energy source

A

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
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2
Q

unique properties of epithelial cells, how these influence transport along nephron

A
  • 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
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3
Q

major pathways of Na+ transport along nephron, how distribution of tranposrters (apical/basal) allow regulation of transport

A

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
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4
Q

proximal tubule Na+ reabsorption

A

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.)

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5
Q

proximal tubule H2O/Cl reabsorption

A

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

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6
Q

thick ascending limb Na+ reabsorption

A

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

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7
Q

distal tubule Na+ reabsorption

A

principal cells of DCT

first portion relies on NCC
second relies on NCC and ENaC

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8
Q

CD Na+ reabsorption

A

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

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9
Q

K+ Reabsorption/secretion basics

A

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

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10
Q

PT K+ reabsorption

A

two paths:

  1. solvent drag k+ reabsorption (early PT)
    - active Na+ reabsorption drives H2O reabsorption, coupled with K+
  2. paracellular diffusion (late PT)
    - positive lumen drives
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11
Q

composition of tubular fluid along PT

A

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

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12
Q

TAL K+ reabsorption

A

2 paths:

  1. transcellular K+ reabsorption
    - Na/K ATPase provides gradient for NKCC2
    - basolateral KCC and K+ channels
  2. paracellular diffusion
    - some K+ needs to be recycled to tubular lumen, creates lumen-positive voltage, drives diffusion
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13
Q

DCT K+ Secretion

A

KCC located apically = major pathway
couples basolateral NA/K ATPase activity to apical K+ transport

DCT late secretion relies on apical KCC and ROMK

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14
Q

CD K+ handling, normal/elevated VS low levels K+

A

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.

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