Transport of Sodium and Chloride 1 and 2 Flashcards

1
Q

How much of the sodium and chloride of the glomerular filtrate is reabsorbed in the proximal tubule?

A

55-65%

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2
Q

types of active transport in the neprhon

A

ATP-dependent

Co- and counter-transport

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3
Q

types of passive transport in the nephron

A

facillitated diffusion

channel-mediated diffusion

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4
Q

NA+/K+ ATPase

A

uses ATP to transport 3 Na+ out and 2 K+ into the cell

always located in the basolateral membrane

allows sodium to be the major energy currency of tubule cell transport

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5
Q

co- and counter-transport

A

transporters that couple favorable movement of sodium and/or potassium to move other ions and solutes

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6
Q

transcellular transport

A

solutes are taken up at the apical surface of the cell and traverse the cytoplasm and are excreted at the basolateral surface into the bloodstream

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7
Q

paracellular transport

A

ions/solutes flow between tubule cells

the driving force for paracellular flux comes from the lumenal vs. basolateral electrochemical gradient

extent depends on number and orcanization of tight junctions

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8
Q

What is the advantafe of a large paracellular flux?

A

mitigates against the formation of large electrical and chemical gradients

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9
Q

solvent drag

A

the process where bulk flow can carry ions and solutes against their graidents

occurs during massive water flux, particularly in the proximal tubule

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10
Q

paracellin-1

A

an Mg2+ channel located between cells of the thick asending limb and distal tubule

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11
Q

What are the reference points for membrane potentials?

A

outside the cell for transmembrane

interstitial for across lumen and interstitium

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12
Q

membrane potential in the presence of leaky tight junctions

A

the tubule cell behaves like an isolated cell

the voltage across each piece of membrane, apical or basal, is the same

transepithelial voltage = 0 mV

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13
Q

membrane potential in the presence of tight tight junctions

A

ionic conductances in the apical and basal membranes sum separately

basal K+ channels set voltage to -70 mV and apical Na+ channels set transmembrane voltage to +70 mV

transepithelial voltage = -140 mV

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14
Q

solute selectivity of the paracellular pathway

A

based on size

the cut-off can be in the 100s of mw

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15
Q

ion selectivity of the paracellular pathway

A

based on charge

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16
Q

resistance of the paracellular pathway

A

varies with the number of rows of junction proteins

increases along the tubule

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17
Q

What is the NaCl concentration in glomerular filtrate?

A

142 mM NaCl

18
Q

What is the concentration of NaCl that the kidney excretes?

19
Q

What is the consequence of having leaky paracellular contacts in the proximal tubule?

A

the uptake becomes iso-osmotic

the solution that leaves the tubule has a similar ionic concentration to that entering the tubule

as a result, there is much less solution leaving and thus less total NaCl

20
Q

proximal tubule sodium transcellular re-uptake mechanisms

A

apical cotransporters for glucose, amino acids, and other metabolites

apical Na+/H+ antiporter

basaolateral Na+/K+ ATPase

basolateral Na+/HCO3- transporter

21
Q

proximal tubule sodium paracellular re-uptake mechanisms

A

osmotic gradient created by Na+ and HCO3= draws water from the lumen, carrying Na+ via solvent drag

22
Q

proximal tubule transcellular Cl- re-uptake mechanisms

A

little or none in the first part of the proximal tubule, where Cl- in the lumen is increased from 115 to 135 mM

in the late proximal tubule, Cl- is unfavorably taken up at the apical surface through an electroneutral Cl-/anion counter-transporter

basolateral transport passively via an ion channel

basolateral transport coupled to a favorable K+ efflux

23
Q

What are the possible anions in the late proximal tubule for chloride cotransport?

A

formate, OH-, HCO3-, and oxalate

24
Q

proximal tubule paracellular Cl- re-uptake mechanisms

A

small amount occurs in the early proximal tubule via solvent drage promoted by the -3mV gradient across the tubule cell tight junctions

significant uptake in the late proximal tubule favored by an increased lumen to blood Cl- gradient

25
active mechanisms for changing or regulating the amount of re-uptake in the proximal tubule
feedback from vascular or renal transmitters play a neglifible role
26
passive mechanisms for changing the amount of re-uptake in the proximal tubule
glomerulotubular balance is a passive mechanism that maintains a constant fraction of Na+ and water re-uptake regardless of overall flow the total amount of Na+ changes with tubular flow by the end of the prixmal tubule, but not the concentration
27
What happens to tight junctions starting with the tDLH?
they become tighter and reduces non-specific paracellular flow
28
function of the thick ascending limb
creates a dilute or concentrated urine impermeable to water concentration depends on presence of water channels in the collecting ducts
29
transcellular mechanisms of ion transport in the TAL
an apical Na+/K+/Cl- transporter an apical Na+/H+ antiporter basolateral Na+/K+ ATPase
30
What drugs inhibit the Na+/K+/Cl- cotransporter and what is the effect?
bumetanide and furosemide (loop diuretics) dilutes medullary interstitium and increases amount of osmotically active Na+ in the collecting duct fluid
31
paracellular mechanisms of ion transport in the TAL
50% of Na+ leaves due to the +15 mV transcellular potential no paracellular Cl- permeability
32
How is the positive potential created in the TAL?
relative impermeability of the tight junctions K+ channel creates a -70 lumen vs intracellular potential K+ and Cl- channel creates a -55mV intracellular vs. interstitial potential result is a positive trans-epithelial potential
33
function of the DCT
further reduces tubule Na+ and Cl- concentrations to a minimum of 40 mM
34
mechanisms of ion transport in the DCT
transcellular is the major mechanism Na+ and Cl- taken up at the apical surface by a co-transporter driving force is the Na+ chemical gradient established by the basolateral Na+/K+ ATPase basolateral chloride channel leads to Cl- efflux due to the negative potential
35
What drug inhibits the Na+/Cl- transporter in the DCT?
thiazide diuretics
36
function of the CCT and MCD
receives remaining 3% of NaCl takes up Na+ to balance the sodium intake
37
mechanisms of ion transport in the CCT and MCD
principal cells move move sodium into the interstitum through EnaC sodium channels (voltage dependent K+ channels on both membranes to prodice a -70 mV potential across the basolateral membrane and -30 mV across the apical membrane paracellular Cl- uptake and Cl-/HCO3- exchanger in beta-interacalated cells
38
regulation of sodium uptake in the CCT and MCD
decreased renal perfusion stimulates release of renin from juxtaglomerular cells this leads to the renin-angiotensin-aldosterone cascade that produces aldosterone alodsterone up-regulates Na+ and K+ channels and aslo the ATPase in principal cells, increasing Na+ reuptake
39
loop diuretics
blocks the Na/K/Cl transporter in the TAL indirectly leads to hypokalemia increased concentration of Na+ flows into the collecting tubule, leading to increased Na+ entry via Na+ channels, which is balanced by K+ efflux
40
thiazide diuretics
blocks the Na/Cl transporter in the DCT wekaer than loop diuretics because only 3-5% of Na+ absorption occurs in the DCT promote Na+ loss, water loss, and hypokalemia
41
potassium-sparing diuretics
directly blocking principal cell Na+ channel in the CCT (amiloride, triamterine) antagonizing aldosterone (spironolactone) - channel removal small effect on Na+ absorption, does not result in increased Na+ influx, so K+ release is not increased