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Renal > Transport of Sodium and Chloride 1 and 2 > Flashcards

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?

A

120 mM

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
Q

active mechanisms for changing or regulating the amount of re-uptake in the proximal tubule

A

feedback from vascular or renal transmitters play a neglifible role

26
Q

passive mechanisms for changing the amount of re-uptake in the proximal tubule

A

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
Q

What happens to tight junctions starting with the tDLH?

A

they become tighter and reduces non-specific paracellular flow

28
Q

function of the thick ascending limb

A

creates a dilute or concentrated urine

impermeable to water

concentration depends on presence of water channels in the collecting ducts

29
Q

transcellular mechanisms of ion transport in the TAL

A

an apical Na+/K+/Cl- transporter

an apical Na+/H+ antiporter

basolateral Na+/K+ ATPase

30
Q

What drugs inhibit the Na+/K+/Cl- cotransporter and what is the effect?

A

bumetanide and furosemide (loop diuretics)

dilutes medullary interstitium and increases amount of osmotically active Na+ in the collecting duct fluid

31
Q

paracellular mechanisms of ion transport in the TAL

A

50% of Na+ leaves due to the +15 mV transcellular potential

no paracellular Cl- permeability

32
Q

How is the positive potential created in the TAL?

A

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
Q

function of the DCT

A

further reduces tubule Na+ and Cl- concentrations to a minimum of 40 mM

34
Q

mechanisms of ion transport in the DCT

A

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
Q

What drug inhibits the Na+/Cl- transporter in the DCT?

A

thiazide diuretics

36
Q

function of the CCT and MCD

A

receives remaining 3% of NaCl

takes up Na+ to balance the sodium intake

37
Q

mechanisms of ion transport in the CCT and MCD

A

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
Q

regulation of sodium uptake in the CCT and MCD

A

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
Q

loop diuretics

A

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
Q

thiazide diuretics

A

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
Q

potassium-sparing diuretics

A

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

Renal (28 decks)

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