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Tubular Function Flashcards

week 7

1
Q

Regulation of Na reabsorption

A

Tuboglomerular feedback (macula densa)

Glomerulartubular balance

Pressure natriuresis

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2
Q

2 step process of Na reabsorption.

A
  1. Movement down across apical membrane concentration and electrochemical gradient using Na+/K+ATPase.
  2. Movement across basolateral membrane against electrochemical gradient using Na+/K+ATPase against high ECF Na.
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3
Q

How is Na mainly Reabsorption in the PCT?

A

Primarily RB using HCO3 then NHE

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4
Q

PCT transporters of Na

A

Na/H+

Na+ glucose

Na+ AA symporter

Na+ Pi symporter

Na Lactate symporter

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5
Q

why is reabsorption of Na in PCT mainly iso-osmotic?

A

coupling of Na and water: water follows

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6
Q

TAL Na Reabsorption

A

No active Na transport

Highly metabolically active so Na-2CL-transporter uptakes Na+

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7
Q

Early DCT Nareabsorption

A

= Na-2Cl-K transport and Na-Cl symporter

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8
Q

Late DCT na reabsorption

A

= ENaCs

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9
Q

What is the impact of increased SNS on Na reabsoprtion?

A

Increased = decreased NaCl excretion = decreased GFR = renin secretion = increased Na reabsorption

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10
Q

Affect of ANG2 on Na reabsorption

A

Increased Na reabsorption via PCT

Stimulates aldosterone and ADH secretion

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11
Q

Affect of ADH on Na reabsorption

A

Increased Na reabsorption in TAL via Na-Cl-K

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12
Q

Affect of Aldosterone on Na reabsorption

A

Acts in principal cells of cortical collecting tubule = increased reabsorption

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13
Q

Affect of ANP on Na reabsorption

A

Acts in principal cells of CD = decreases Na reabsorption

Decreases in DCT and CD via ENaCs

Inhibits Na Reabsorption in PCT

Inhibits renin

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14
Q

Affect of increased Na intake

(four main)

A

increased ECF and EABV –>

a) decreased SNS –> dilation of aff arterioles –> decreased Na R (PCT)

b) increased ANP –> constriction of efferent arterioles –> decreased Na R (CDs)

c) decreased colloid osmotic pressure –> decreased Na reabsorption (PCT)

d) deceased RAAS –> decreased Na reab (PCT and CD)

= increased Na excretion

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15
Q

Glucose Reabsorption - where?

A

100% in PCT via secondary active transport

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16
Q

how is glucose reabsorbed?

A

1st half: apical membrane = SGLT (1:1), basolateral = GLUT2

2nd half: apical = SGLT1 (2:1), basolateral = GLUT1

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17
Q

What factors influence glucose reabsorption?

A

plasma glucose level

Tubular load of glucose

Sodium load in the proximal tubule

Sodium-glucose transporters/ # glucose transporters (transporter saturation)

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18
Q

Transport Maximum

A

Plasma level or filtration load substance at which carriers are completely saturated.

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19
Q

What happens when a transport max reached for all nephrons?

A

When reached in all nephrons further increases are not reabsoprbed = excretion of that substance

20
Q

Renal Threshold

A

Tubular load at which transport maximum is exceeded in SOME nephrons.

21
Q

Transport max and renal threshold of glucose

A

TM= 350mg/D/L

RT= 180mg/dL

22
Q

What happens when plasma glucose levels exceed the renal threshold?

A

filtered load > reabsorbing capacity of PCT

- % of filtered glucose that is reabsorbed decreases

- % of the filtered load of glucose that is excreted in the urine increases (glycosuria)
23
Q

Hypo, hyper and normal range of K

A

Hypo= <3.5Eg/L

Hyper = >5.0Eg/L

Normal = 4Eg/L

24
Q

Where is K reabsorbed?

A

67% in PCT
20% in TAL

25
K reabsorption in PCT
paracellular
26
K reabsorption in DCT and CD
A-intercalated cells (low K diet) = apical H+/K+ATPase, K+ channels and BK channels Principal cells (normal --> high K diet) = K+ from blood --> lumen, diffusion across luminal membrane
27
K reabsorption in TAL
K+ reab via Na-2Cl-K cotransporter May diffuse into lumen
28
Aldosterone and K reab
Increased intracellular K+ concentration gradient for K+ secretion via ROMK also increased luminal K+ channels in principal cells
29
Alkalosis and Acidois on K reab
Alkalosis Increased K secretion Acidosis Decreased K secretion
30
What is the impact of Thiazide on K reab?
blocks Na+Cl in DCT --> decreased Na reab in DCT --> increased NA into CD --> increased Na w ENaes --> imcreased K+ secretion
31
what form is Ca in kidneys?
Free form Ca2+ Bound (not filtered) complex form
32
Where is Ca reab?
PCT (67%) DCT (8%)
33
How is Ca reab in PCT?
2/3 paracellular, 1/3 transcellular Apical Ca channels Basolateral Ca2+ATPase or Na/Ca exchanger
34
How is Ca reab in TAL?
Paracellualr reab from Na-2Cl-K
35
How is Ca reab in DCT?
By PMCA and NCX
36
Thiazide diuretics and Ca reab
T --> blocked NaCl symporter --> decreased Na inside DCT -->increased NaCa exchange --> increased Ca reab --> decreased Ca (loss in urine)
37
loop diuretics and Ca reab
- inhibits Na-2Cl-K cotransporter --> decreased K secretion --> decreased lumen positivity --> decreased Ca2+ reabsorption
38
PTH and ca reab
increases Ca reab in TAL, late DCt and early CD
39
Vit D and Ca reab.
increased Ca reab in TAL and DCT
40
increased free Ca impact on Ca reab?
TAL cells express basolateral CaSR Increased uptake due to larger potential difference
41
calcitonin and Ca
decreased Ca reab
42
What proteins are filtered?
- peptide hormones - small proteins - albumin (small amounts)
43
Where are proteins reab and how?
PCT endocytosis
44
What proteins mediates endocytosis and reab?
megalin and cubilin
45
What are the three types of batter Syndrome and what channels are affected in each?
1- Na-2Cl-K symporter 2- Apical K+ channel (ROMK) 3- Basolateral Cl- channel
46
What is batter syndrome
Set of autosomal recessive genetic diseases w hypokalaemia, metabolic alkalosis and hyperaldosteronism. all inactivating mutations

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