Renal Lectures 2 and 3 Flashcards

1
Q

Which part of the tubule reabsorbs most of filtered fluids?

A

The proximal tubule reabsorbs 67% of filtered water and Na, K, Cl and other solutes. Key element of this is Na+ K+ ATPase.

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2
Q

How does ion concentration differ as the fluids travel the proximal tubule?

A

In 1st have of proximal tubule, Na is reabsorbed with HCO3- (H+).
In 2nd half of proximal tubule, Na is reabsorbed with Cl-.
Na in will be greater then Na out making a steep chemical gradient.

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3
Q

Paracellular route

A

Tight junctions -> passive diffusion

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4
Q

Transcellular route

A

Active transport through cell, includes transapical, transbasal, and translateral pathways

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5
Q

What drives the Na intro the cells and out of the lumen

A

Electrochemical gradient - cell interior negative. Na into cell is passive.

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6
Q

Is Na from cell to interstitial space passive or active

A

Active

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7
Q

Is Na backleak through tight junctions from cell to lumen passive or active

A

Passive

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8
Q

Describe sodium transport along the nephron

A

Early proximal tubule - sodium and bicarbonate absorbed
Late proximal tubule - sodium and chloride ions absorbed
Ascending limb - NaCl absorbed
Distal tubule - NaCl absorbed
Collecting duct - NaCl absorbed

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9
Q

How is sodium reabsorbed in early proximal tubule

A

Na/H exchanger and Na-solute cotransporter

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10
Q

How is sodium reabsorbed in late proximal tubule

A

Apical sodium transporters: parallel exchangers and Na/H and Cl/base

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11
Q

How is sodium reabsorbed in thick ascending limb

A

Apical sodium transporter - Na/K/2Cl triporter

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12
Q

How does proximal fluid composition change along proximal tubule

A
  1. Chlorine rises and plateaus
  2. Na stays consistent
  3. Pi drops and plateaus
  4. HCO3-, Glucose, and Lactate drop even further - depletion of major solute
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13
Q

How is sodium reabsorbed in the early distal tubule

A

Apical sodium transporter - NaCl cotransporter

This is anti-natuiretic - decreases sodium excretion by anti natuiretic agents

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14
Q

How is sodium reabsorbed in the late distal tubule and collecting duct

A

Apical sodium transporter - Epithelial sodium channel.

Na absortion to principal cell.

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15
Q

How do angiotensin and NE affect sodium reabsorption

A

Increases absorbtive capacity
Stimulate Na/H transporter
Innervated with sympathetic activity

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16
Q

Describe the apical effect of Na entry by NE and AII

A

NE -> a2 receptor -> Gai
AII -> AT1 receptor -> Gai
Results in decrease cAMP concentration, decrease PKC activity, stimulates Na/H exchanger

17
Q

Describe the basolateral effect of Na extrusion by NE

A

NE-> a1 receptor -> Gaq

Activates PLC to increase intarcellular Ca2+ concentration and stimulate Na/K ATPase

18
Q

Aldosterone

A

Modulates sodium transport in principal cells by increasing sodium absorption. It binds to the mineralcorticoid receptor and migrates to nucleus to produce protein which can be used to make channels and also stimulates mitochrondria to make ATP. It is an anti-naturietic agent - increases absorption.

19
Q

Atrial Natriuretic Peptide (ANP)

A

Targets principal cell to block Na uptake -> urine volume increases.
Increases CGMPby binding to its receptor. Increased CGMP inactivates epithelial sodium channel by
1. binding to an allosteric modifer site on the channel
2. phosphorylating the channel via cGMP-dependent PK.

20
Q

Diuretics

A

Increase in sodium excretion by target specific transport system
Decreased absorption, increeased urine

21
Q

Which sections of the nephron are water impermeable

A

Thick ascending limb, early distal tubule, collecting duct

22
Q

Where is very dilute urine found in nephron

A

After TAL and around early distal tubule, Na gone but water not yet reabsorbed

23
Q

How does ADH affect water transport along the nephron

A

More dilute in late distal tubule and medulary collecting duct because ADH makes cells more water permeable.

24
Q

Mode of action of ADH

A

ADH, aka vasopressin, creates water channels.

25
Q

Describe distribution and balance of potassium

A

Most K+ is reabsorbed and in intracellular compartment (90%). Small percentage in feces and urine.

26
Q

These stimulate K+ exchange into the ICF while Na goes out (ATPase pump)

A

Epinephrine released from adrenal gland and insulin from pancreas; both released due to increased extracellular K+.

27
Q

Describe reabsorption of K+ in the nephron for a diet low in potassium

A

80% reabsorbed in proximal convuluted tubule
10% reabsorbed in thick ascending limb
Only 2% of filtered load remaining in collecting duct

28
Q

Describe reabsorption of K+ in the nephron with a healthy amount of K+ in diet

A

80% reabsorbed in proximal convuluted tubule
10% reabsorbed in thick ascending limb
20-180% secreted by initial collecting tubule
10-150% of filtered load remaining in collecting duct

29
Q

K+ transport in proximal tubule

A

K+ channel (K out)
K+/Cl- symporter (K out)
Na/K exchanger (K in)

30
Q

K+ transport in thick ascending limb (TAL)

A

Na/K Cl symporter (K in)
K channel (K out)
Na/K antiporter (L in)

31
Q

K+ transport in Cortical collecting tubule (CCT): alpha-intercalated cell

A

Na/K antiporter (K in)
K/H antiporter (K in - therefore increased pH / more basic extracellularly)
K channel (out)

32
Q

K+ transport in cortical collecting tubule: principal cell

A

Passive K channel out

Active K/Na pump exchanger K in

33
Q

Increased plasma K+ concentration

A

Increasing K+ secretion, to a plateau

34
Q

Tubular flow rate to K+ secretion

A

Higher tubular flow rate = higher K+ secretion rate

35
Q

A diet (high/low) in K+ has a higher secretion rate per same tubular flow rate

A

High

36
Q

How is K+ regulated by pH

A

Increase in pH (more basic) = steeper increase in K+ secretion.

37
Q

How is K+ regulated by aldosterone

A

Increase in aldosterone = increase in secretion of K+