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renal > A. TUBULAR FUNCTION > Flashcards

A. TUBULAR FUNCTION Flashcards

1
Q

what is unique about each tubular segment of the nephron

A

they each express different channels/transporters and hence have different properties

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2
Q

what barriers does the filtrate have to cross to be reabsorbed into plasma of peritubular capillaries (tubule to blood)

A
  • apical/luminal membrane
  • cytosol of tubular cell
  • basolateral membrane
  • interstitial fluid
  • capillary wall of peritubular capillaries
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3
Q

what tubular cells polarised or non-polarised

A

polarised

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4
Q

what are different ways molecules can move out of the filtrate

A
  • transcellular (through the cell) by diffusion or actively
  • paracellular diffusion (through tight junctions)
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5
Q

what molecules can pass through the membrane by passive diffusion

A
  • lipophilic molecules eg - steroid hormones
  • gases
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6
Q

what is diffusion

A
  • passive as no energy involved
  • down concentration gradient or electrochemical gradient
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7
Q

how does water diffuse across membranes

A

osmosis: net movement or diffusion of solvent molecules through a selectively-permeable membrane from a region of high water potential to a region of low water potential

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8
Q

what molecules pass by simple diffusion

A
  • gases
  • lipophilic molecules
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9
Q

what molecules pass by facilitated diffusion through channels and carriers

A

hydrophilic molecules

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10
Q

what is active transport

A
  • against a concentration or electrochemical gradient
  • primary: coupled directly to an energy source (eg hydrolysis of ATP)
  • secondary: coupled indirectly to an energy source
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11
Q

what is the transport maximum, Tm

A
  • capacity of carrier exceeded ie - fully saturated
  • so remaining of solute is stays in filtrate and isn’t transported
  • eg: glucose transporter is saturated in diabetes causing glycosuria and osmotic diuresis
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12
Q

role of PCT

A

primary site of reabsorption for all solutes, dependent on the action of Na+/K+ ATPase

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13
Q

what is reabsorbed from the PCT into the blood

A
  • Na+, Cl-, K+, HCO3
  • glucose
  • water
  • urea
  • amino acids
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14
Q

what is secreted from blood into PCT

A

organic acids/bases
mainly an active process:
- organic anion (OA-) transport (e.g. bile salts, urate/ uric acid)
- organic cation (OA+) transport (e.g. adrenaline, NA, dopamine)
- drugs include diuretics (OA-), penicillins (OA-), opioids (OA+)

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15
Q

what antiporter is on the basolateral membrane in the PCT

A
  • Na+-K+ ATPase pump (carrier)
  • 3 Na+ out of the tubular cell
  • 2 K+ from interstitial fluid into the tubular cell
  • hydrolyses ATP to ADP (primary active transport)
  • low to high concentration (against conc grad)
  • tubular cell becomes more negative
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16
Q

what antiporter is on the apical membrane in the PCT

A
  • Na+/H+ antiporter
  • secretion of H+ (from water) from tubular cell to tubule lumen
  • against conc grad
  • secondary active transport
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17
Q

what symporter is in the basolateral membrane in the PCT

A
  • HCO3-/Na+
  • net effect is reabsorption of HCO3-
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18
Q

what symporter is in the apical membrane in the PCT

A
  • Na+/glucose symporter (SGLT-2)
  • also Na+/ amino acid symporter
    (secondary active transport)
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19
Q

what transporter is in the basolateral membrane in the PCT

A
  • GLUT-2 transporter
  • facilitated diffusion
  • down conc grad (high to low)
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20
Q

what channel is in the basolateral membrane in the PCT

A
  • K+ channel
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21
Q

passive reabsorption of water in PCT

A
  • by osmosis
  • through ‘leaky’ tight junctions and via water channels, aquaporins (trans cellular)
  • high water permeability
  • also facilitated by osmotic gradient caused by Na+ reabsorption
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22
Q

passive reabsorption of Ca2+, Cl- and K+ (some Na+) in PCT

A
  • by paracellular transport, as a result of active reabsorption of Na+ at basolateral membrane
23
Q

passive reabsorption of urea in PCT

A
  • 50% of urea is reabsorbed
  • indirectly linked to Na+ reabsorption
  • reabsorption of water secondary to Na+ reabsorption creates a concentration gradient that favours passive reabsorption of urea due to conc urea in filtrate
  • reabsorbed down conc grad from high to low
24
Q

role of loop of henle

A
  • NaCl and water reabsorption
  • creation of hyperosmotic renal medullary interstitium
    which provides osmotic gradient for water reabsorption
  • controls concentration of urine
25
Q

what forms the juxtaglomerular apparatus

A

macula densa cells (tubular) and juxtaglomerular granular cells (vascular)

26
Q

where is the juxtaglomerular apparatus located

A

where the DCT passes the fork formed by afferent and efferent arterioles

27
Q

what is the role of the macula densa cells

A

(tubular cells)
- detect conc of NaCl in tubular fluid
- involved in the tubuloglomerular feedback mechanism

28
Q

what is the role of juxtaglomerular granular cells

A

(modified SM cells)
- secrete renin
- present in the vascular component
- most numerous in theafferent arteriole
- involved in the tubuloglomerular feedback mechanism

29
Q

how can the kidneys auto regulate rapidly

A
  • they change blood pressure by adjustment of the diameter of the afferent arteriole by:
    1. myogenic properties of arterioles: intrinsic, ie will resist stretch of vascular walls if BP too high
    2. tubuloglomerular feedback
30
Q

tubuloglomerular feedback with increased arterial pressure

A
  • increased GFR due to increased glomerular hydrostatic pressure and hence increased net pressure
  • increases flow rate in loop of Henle so less time for Na+ and Cl- reabsorption in LoH
  • conc of NaCl at macula densa cells is increased
  • sensed by macula densa cells at top of ascending limb of LoH
  • macula densa cells secrete vasoconstrictive agents:
    endothelin
    adenosine (more likely)
    ATP (more likely)
  • through paracrine signalling: into IF, transferred in IF to granular cells and SM cells of afferent and efferent arterioles
  • causes an increase in resistance to blood flow (decreased) in afferent arterioles (vasoconstriction) returning GFR towards normal
31
Q

myogenic activity with increased blood pressure

A
  • stretching of blood vessels is resisted by SM cells by narrowing of afferent arteriole (VC)
  • decreased blood flow
  • decreased hydrostatic pressure
  • decreased GFR
32
Q

TGF activity with increased blood pressure

A
  • adenosine/ATP reaches SM cells of afferent arteriole causing VC etc
33
Q

tubuloglomerular feedback with decreased arterial pressure

A
  • decreased GFR due to decreased glomerular hydrostatic pressure and hence decreased net pressure
  • decreases flow rate in loop of Henle so more time for Na+ and Cl- reabsorption in LoH
  • conc of NaCl at macula densa cells is decreased
  • sensed by macula densa cells at top of ascending limb of LoH
  • macula densa cells secrete vasodilatatory agents:
    PGs: PGE1, E2, I2
    Bradykinin
    NO (most likely)
  • through paracrine signalling: into IF, transferred in IF to granular cells and SM cells of afferent and efferent arterioles
  • causes a decrease in resistance to blood flow (increased) in afferent arterioles (vasodilatation) returning GFR towards normal
34
Q

myogenic activity with decreased blood pressure

A
  • less stretched so there is relaxation of afferent arteriole to maintain good blood flow
35
Q

TGF activity with decreased blood pressure

A
  • NO causes vasodilation?
36
Q

angiotensin II causing vasoconstriction with decreased blood pressure

A
  • macula densa cells communicate to juxtaglomerular cells
  • increased renin release from granular cells of afferent and efferent arterioles
  • renin stimulates angiotensin II production causing vasoconstriction of efferent arterioles, thus returning GFR towards normal
37
Q

role of the early DCT

A
  • reabsorbs Na+, K+, Cl-, Ca+ but is virtually impermeable to water and urea
38
Q

what antiporter is on the basolateral membrane in the early DCT

A
  • Na+-K+ ATPase pump (carrier)
  • 3 Na+ out of the tubular cell
  • 2 K+ from interstitial fluid into the tubular cell
  • hydrolyses ATP to ADP (primary active transport)
  • low to high concentration (against conc grad)
  • tubular cell becomes more negative
  • creates grad for reabsorption of Na+ down its conc grad with Cl-
39
Q

what symporter is in the apical membrane in the early DCT

A
  • Na+-Cl- symporter
  • Na+ and Cl- enter tubular cell
40
Q

what channels are present in basolateral membrane of early DCT

A
  • Cl- channel
  • K- channel
  • both enter interstitial fluid
41
Q

what is the late DCT and CD composed of

A
  • principal (P) and intercalated (I) cells
  • P-cells reabsorb Na+, Cl-, water and secrete K+
  • I cells reabsorb K+ and HCO3- and secrete H+
42
Q

what antiporter is present in basolateral membrane of P-cells

A
  • Na+-K+ ATPase pump (carrier)
43
Q

what channels are present in basolateral membrane of P-cells

A
  • Cl- channel
  • K+ channel
  • both enter interstitial fluid
44
Q

what channels are present in apical membrane of I-cells

A
  • Na+ selective channels (ENaC)
  • enters tubular cell by passive diffusion as Na+ low (reabsorbed)
  • K+ channel
  • enters tubular lumen (secreted)
45
Q

what hormones take action in P-cells

A
  • aldosterone (increase Na+ and water reabsorption and K+ secretion)
  • ADH (increase permeability to water so increased reabsorption)
46
Q

what transporter is in the basolateral membrane of I cells

A
  • HCO3- carrier (transporter)
  • K+ channel
  • both enter interstitial fluid
47
Q

what pump is in apical membrane of I-cells

A

H+-ATPase
- H+ pumped out against its own grad

48
Q

what antiporter is in apical membrane of I-cells

A
  • K+/H+-ATPase
  • K+ into tubular cell and H+ into tubular lumen
49
Q

what effect does aldosterone have in I cells

A

stimulates H+ secretion

50
Q

% of Na+ reabsorbed in different segments of nephron

A

65% from PCT
25% from LoH
5% from DCT
5% from CT
<1% excreted in urine

51
Q

% of K+ reabsorbed in different segments of nephron (low intake)

A

65% from PCT
20% from LoH
5% from DCT
10% from CT
<1% excreted in urine

52
Q

% of K+ reabsorbed in different segments of nephron (high intake)

A

65% from PCT
20% from LoH
10-50% kept in DCT
5-30% kept in CD
15-80% excreted in urine

53
Q

% of glucose reabsorbed in different segments of nephron

A

98% from PCT
2% beyond PCT
0% excreted as we want to keep glucose to use as energy

54
Q

% of glucose reabsorbed in different segments of nephron (plasma glucose conc ≥10mmol/L)

A

Tm for glucose reabsorption is exceeded, glucose appears in urine
ie - Na+/glucose co-transporters saturated in PCT

renal (13 decks)

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