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BMS 615 Cardiovascular > Test2: Wk6: 3 Tubular Transport of NaCl - Mangiarua > Flashcards

Test2: Wk6: 3 Tubular Transport of NaCl - Mangiarua Flashcards

1
Q

Proximal Tubule Na Reabsorption

A

Na/H Antiport 65%

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2
Q

Thin Descending Limb Na Reabsorption

A

0%

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3
Q

Thin Ascending Limb Na Reabsorption

A

0%

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4
Q

Thick Ascending Limb Na Reabsorption

A

Na-K-2CL multiport, paracellular diffusion

25%

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5
Q

Distal Tubule Na Reabsorption

A

Na-Cl symport

5%

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6
Q

Collecting Duct Na Reabsorption

A

Na Channels
5%
Varies depending on Na intake

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7
Q

Na and water freely filtered at the

A

renal corpuscle

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8
Q

Na in bowmans space is – as plasma

A

same

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9
Q

Na is reabsorbed along —

A

the entire nephron

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10
Q

% Na excreted

A

<1%

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11
Q

Na is — into the interstitium

A

actively extruded

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12
Q

Na enters — from the tubular lumen

A

passively

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13
Q

— follow Na

A

anions

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14
Q

— follows solute

A

water

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15
Q

water and solutes move by — into —

A

bulk flow into peritubular capillaries

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16
Q

Na movement across the basolateral membrane is

A

uphill, by Na-K-ATPase

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17
Q

Na movement across the luminal membrane is

A

downhill

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18
Q

Major site of salt and water reabsorption

A

entire proximal tubule

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19
Q

In proximal tubule, Na entry is coupled with — ions using the —

A

H, NHE3 antiporter

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20
Q

Proximal tubule - Additional Na enters in symport with (3)

A

with glucose, amino acids, and phosphate.

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21
Q

Proximal tubule - Na is transported to the interstitium mostly via the basolateral — and symport with —

A

Na,K-ATPase; bicarbonate.

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22
Q

Proximal tubule - Cl that enters in antiport with organic base leaves mostly via — with a substantial amount reabsorbed —

A

channels; paracellularly

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23
Q

Proximal tubule - Water moves paracellularly and intracellularly via —

A

aquaporins.

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24
Q

Glomerulotubular balance - changes in GFR is — to filtered load of Na

A

proportional; always 2/3rds

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25
Q

Glomerulotubular balance - the proximal tubule reabsorbs — of filtered salt and water

A

constant fraction

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26
Q

Glomerulotubular balance - the amount of filtered salt and water that leaves the proximal tubule — as filtered amount —

A

increases, increases

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27
Q

the descending loop of Henle does not reabsorb — but does reabsorb —

A

Na or Cl; water

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28
Q

the ascending loop of Henle reabsorbs — but not —

A

Na and Cl, water

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29
Q

major transporter in thick ascending limb

A

NKCC

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30
Q

thick ascending limb contains — in addition to NKCC

A

ROMK

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31
Q

thick ascending limb - ROMK function

A

recycle K from the cell interior to the lumen and to the interstitium

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32
Q

thick ascending limb Na can also move — in response to the —

A

paracellularly; lumen positive potential

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33
Q

thick ascending limb water reabsoprption

A

not reabsorbed

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34
Q

Bartter’s syndrome

A

mutations of genes encoding proteins that transport ions
in the thick ascending limb of the nephron, including the Na-K-2Cl cotransporter, the K+
channel, and the Cl- channel.

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35
Q

% Na and %Cl that reach distal tubule

A

10% and 20%

36
Q

distal tubule transporter

A

NCC

Na-Cl symporter

37
Q

Gitelman’s syndrome

A

mutations in the gene that codes for the Na-Cl

cotransporter in the distal tubule.

38
Q

Gitelman’s syndrome characterized by

A

It is characterized by increased excretion of Na+, Mg2+, Cl-, and K+.

39
Q

Bartter’s syndrome characterized by

A

Very large urinary losses of NaCl, hypokalemia. Ca2+ and Mg2+ wasting may also occur

40
Q

Cortical collecting duct Na reabsoprption

A

apical Na Channels

41
Q

apical Na channels controlled by

A

aldosterone

42
Q

Cortical collecting duct water reabsorption

A

aquaporins

43
Q

aquaporins controlled by

A

ADH

44
Q

Liddle’s syndrome

A

mutations in the gene that codes for the epithelial sodium channel in the principal cells of the collecting duct system inducing excess Na+ reabsorption

45
Q

Liddle’s syndrome characterized by

A

early, and severe
hypertension associated with low plasma renin activity, metabolic alkalosis due to
hypokalemia, and hypoaldosteronism.

46
Q

4 ways reabsorption of Na drives reabsorption of other substances

A
  1. create lumen negative transtubular potential difference across the epithelium - diffusion
  2. Creates transtubular osmolarity difference - osmosis
  3. reabsorption of many organic nutrients, phosphate, and chloride by
    cotransport.
  4. secretion of hydrogen ion (in the proximal tubule) by countertransport - bicarbonate
47
Q

chloride reabsorption Proximal tubule

A

Paracellular diffusion in mid-to-late portions; driving force is high luminal chloride
concentration caused by water reabsorption.

48
Q

chloride reabsorption Thick ascending loop

A

Secondary active via Na,K,2Cl transporter in luminal membrane.

49
Q

chloride reabsorption Distal convoluted tubule (2)

A

(1) Paracellular diffusion; driving force is lumen-negative PD;
(2) Secondary active via Na,Cl cotransporter in luminal membrane.

50
Q

chloride reabsorption Cortical collecting duct (2)

A

(1) Paracellular diffusion; driving force is lumen-negative PD;
(2) Secondary active via HCO3-,Cl countertransporter in luminal membrane (sodium
independent) .

51
Q

9 controllers of Na Reabsorption

A
  1. Glomerular tubular balance
  2. Aldosterone
  3. PC starling forces hydrostatic pressure
  4. Renal SNS nerves
  5. ANGII
  6. Pressure Natriuresis
  7. ANP
  8. ADH
  9. Dopamine
52
Q

Glomerular tubular balance

A

constant proportion of Na reabsorbed

53
Q

most important controller of Na reabsoption

A

Aldosterone

54
Q

Aldosterone is produced

A

in adrenal cortex

55
Q

aldosterone stimulates Na reabsorption in

A

the principal cells of cortical collecting duct

56
Q

Aldosterone functions to

A

retain Na

57
Q

Aldosterone controls % of Na reabsorption

A

2%

58
Q

4 Steps of Aldosterone function

A
  1. Bind intracellular receptors
  2. ⬆ mRNA
  3. ⬆ translation of proteins
  4. ⬆ expression of luminal Na Channels and basolateral Na-K-ATPase pumps
59
Q

Aldosterone action on late distal, cortical, and medullary collecting ducts (3)

A

⬆ Na reabsorption in principal cells
⬆ K secretion in principal cells
⬆ H secretion in intercalated cells

60
Q

(3) stimulate aldosterone secretion

A

ANGII
⬆ plasma K conc.
ACTH

61
Q

(1) inhibits aldosterone secretion

A

ANP

62
Q

most important regulator of Aldosterone

A

ANGII

63
Q

Plasma ANGII conc. is determined by

A

plasma Renin conc.

64
Q

(3) factors that control renin secretion

A

intrarenal baroreceptors
macula densa
renal SNS nerves

65
Q

Peritubular capillary starling forces, hydrostatic pressure, and oncotic pressure influence

A

renal interstitial hydrostatic pressure RIHP

66
Q

⬆ RIHP ➡ — Na and water

⬇ RIHP ➡ — Na and water

A

⬆ RIHP ➡ ⬇Na and water

⬇ RIHP ➡ ⬆ Na and water

67
Q

Renal nerve stimulation stimulates (3)

A
  1. renin secretion
  2. Na reabsorption via direct action on tubular cells
  3. AA and EA constriction
68
Q

Renin secretion is activated by — receptors on — cells

A

Beta1 on granular cells

69
Q

SNS activates tubular cells on the — tubule

A

proximal

70
Q

SNS stimulates AA and EA constriction via — receptor

A

alpha adrenergic

71
Q

ANGII — Na reabsorption by — and —

A

increases, indirect and direct

72
Q

ANGII indirect effects (2)

A

⬆ Aldosterone

⬇ RIHP

73
Q

ANGII direct effects

A

tubular cells - increases tubular Na reabsoption

74
Q

Pressure Natriuresis - when renal arterial pressure increases the kidneys show — with little changes in —

A

rapid increase in Na and water excretion with little changes in GFR

75
Q

3 possible Pressure Natriuresis intrarenal mechanisms

A

⬇ renin
⬆ renal paracrine agents that ⬇ Na reabsorption
⬆ RIHP

76
Q

what causes ANP secretion

A

increased plasma volume resulting in distension of cardiac atria

77
Q

ANP Direct effects (2)

A
  1. acts directly on inner medullary collecting ducts to ⬇ Na reabsorption
  2. cGMP inhibition of luminal membrane Na channels
78
Q

ANP indirect effects (4)

A
  1. granular cells ⬇ renin
  2. adrenal cortex to ⬇ ANG induced aldosterone secretion
  3. AA and EA constriction
  4. Dilation of Mesangial cells
79
Q

dilation of mesangial cells causes

A

⬆ glomerular Kf ➡ ⬆ GFR ➡ ⬆ Na excretion

80
Q

what causes ADH release

A

decreased plasma volume

81
Q

ADH major function

A

increase permeability of cortical and medullary collecting ducts to water

82
Q

ADH also increases

A

Na reabsorption by cortical collecting ducts

83
Q

Dopamine inhibits

A

Na reabsorption

84
Q

Dopamine is synthesized in

A

proximal tubule cells from L-DOPA taken up from renal circulation and glomerular filtration

85
Q

L-DOPA is converted to dopamine where

A

proximal tubule epithelium

86
Q

Dopamine is released to act in a — manner

A

paracrine

87
Q

2 actions of dopamine

A
  1. internalization of NHE antiporters ad Na-K-ATPase pumps to reduce Na reabsoprtion
  2. reduce expression of all receptors to decrease ability of ANGII to stimulate Na reabsorption

BMS 615 Cardiovascular (49 decks)

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