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Flashcards in Salt and water handling Deck (38):
1

Water content in various tissues

Kidney
heart
lung
skeletal muscle
brain
skin
liver
skeleton
adipose tissue

2

Division of TBW

60% body weight
1/3 ECF (20%), 2/3 ICF (40%)
ECF: 1/4 plasma (5%), 3/4 ISF (15%)

3

ISF

fluid in lymphatics
crystallized water in bone
CT
transcellular fluid (intraocular, CSF, synovial, peritoneal, pleural, pericardial fluids)

4

Osmolarity

osmol/L water

5

Osmolality

osmol/kg water

6

ECF solutes

Na+
Cl-, HCO3-

7

ICF solutes

K+
proteins, organic phosphates, acids

8

Plasma water content

93%

9

Normal osmolality

280-300 mosmol/kg water

10

Effective osmoles

Na+
cells
plasma proteins

11

Ineffective osmoles

urea

12

Tonicity

# effective osmoles /solution

13

Starling's forces

Jv = Kf ((Pc - Pi) - (pic-pii))
Pc = hydrostatic pressure in capillaries
Pi = hydrostatic pressure in interstitium
pic = oncotic (colloid) pressure in capillaries
pii = oncotic pressure in interstitium

Colloid pressure is key in maintaining intravascular volume

14

Physiological vasculature fluid movement

Hydrostatic - favours movement out of vasculature
Oncotic - favours retention
Net result = slight movement out of vasculature - absorbed by lymphatics and returned to venous circultaion

15

Causes of edema

Increased vascular permeability
Increased hydrostatic pressure in vasculature
Decreased oncotic pressur
Lymphatic obstruction
Increased oncotic pressure in ISF

16

Glomerulus filtering

freely filters Na+ and Cl-

17

PCT

65% Na+ and H2O reabsorbed

18

Sodium reabsorption in early PCT

Na/K ATPase on basolateral membrane: 3Na out of cell, 2K into cell
Establish a electrical gradient --> allows Na to move down the gradient into the cell

2 mechanisms of Na movement into cells:
1) Na+/H+ exchanger (NHE3):
- H+ generation by dissociation of H2CO3 (generates HCO3-)
- H+ moves into lumen, combines with HCO3- to form H2CO3, which dissociates to CO2 and H2O (carbonic anhydrase)
- CO2 diffuses into cell, gets converted to H2CO3 by carbonic anhydrase
- HCO3- moves into interstitium and is reabsorbed by blood

2) Na+/X- cotransporter
- Na+ moves down concentration gradient along with another solute
- X = amino acids, phosphate, citrate, glucose

Once in the cell, Na/HCO3- move into interstitium via Na/K ATPase and cotransporters
Cl- is not reabsorbed; Cl- concentration rises through this section

19

Sodium reabsorption in late PCT

2 mechanisms:
1) coupled Na/H and Cl/HCO3- antiporters
2) Paracellular passive diffusion

Driven by Cl- concentration gradient (high in lumen) established in early PCT

20

Water reabsorption in PCT

Movement of Na, Cl, HCO3- into interstitium establishes osmotic gradient for water to move out of lumen --> interstitium and into blood
PCT is highly permeable to water, moves from lumen --> blood via paracellular/transcellular pathways

21

Hormones affecting PCT

Angiontensin II: increase water and NaCl reabsorption
Adrenaline/noradrenaline: increase water and NaCl reabsorption
Dopamine: decrease water and NaCl reabsorption

22

Thin descending limb

"concentrating segment"
water permeable, solute impermeable
water moves out of filtrate, increasing concentration of filtrate
15% of water reabsorbed here

23

Thick ascending limb

"Diluting segment"
water impermeable
25% of Na+, Cl-, K+ reabsorbed here

24

Thick ascending limb transporters

NKCC:
- 2 Cl-, 1 Na+, 1K+ into cell from lumen
- Na+ moved into interstitium by Na+/K+ ATPase
- NKCC associated with ROMK: allows K+ to move from cell --> lumen, creates K+ gradient that helps drive NKCC channel
- also established positive charge in lumen, which drives other cations of urine into blood

Na+/H+ exchanger
Paracellular movement of ions

25

Hormonal effects on Loop of Henle

Aldosterone: increase NaCl absorption
Adrenaline: increase NaCl absorption

26

DCT

Reabsorbs ~7% of NaCl
secretes variable amounts of K+ and H+
water impermeable, remains a diluting segment

27

Transporters in DCT

NaCl cotransporter (NCC)
- moves 1 Na+ and Cl- into cell from lumen
- not associated with ROMK, so no electropositivity established in urine to drive other cation diffusion

28

Hormonal regulation of DCT

Aldosterone
Adrenaline
ADH: increase water reabsorption

29

Collecting duct

makes final decisions about salt and water balance
determination of pH in urine

30

Cell types in CD

1) principal cells
- have ENaC (epithelial sodium channels) - moves Na+ into cells from urine
- have ROMK: moves K+ into urine from cell, in response to negative lumen due to sodium movement

2) Intercalated cell
- response for acid-base balance
- determine acid-base balance by secreting/reabsorbing H+ and bicarbonate

31

Hormonal effects in CD

Aldosterone: increase chance of ENaC being open - increase water and NaCl reabsorption
Adrenaline
ADH: increase # of ENaC receptors available, increase water reabsorption
ANP: decrease # ENaC receptors available, decrease water/NaCl reabsorption
Urodilatin: decrease water/NaCl reabsorption

32

Urodilatin

secreted by DT/CD (not present in systemic circulation)
due to increase in ECFV
acts on CD
decrease NaCl/water reabsorption

33

Dopamine

released by dopaminergic nerves in the kidney, also synthesized by cells of PT (oppose action of adrenaline/NA)
Due to increased ECFV
acts on PT to decrease water/NaCl reabsorption

34

Other hormonal regulators

PG: PGI2 mainly
- afferent arteriolar vasodilation + natriuresis
- low ECFV: PGI2 rises to maintain renal perfusion, despite SNS activation & high AII
- giving NSAIDs to these patients can reduce PGI2 levels, cause renal failure

Uroguanylin: released in response to salt intake
- inhibits salt reabsorption in kidneys

NO: some diuretic properties

35

ADH

2 receptors:
V1 - v/c in arterioles, also found in brain/mesangial cells
V2 - CD cells and cause water resorption

Stimulated by:
- increasing osmolality in blood
- volume depletion
- vomiting/diarrhea
- pain
- exercise
- medications (narcotics, chlorpropamide, carbamapezine)

36

Diluting urine

Solute reabsorption without water
- ascending limb
- DT and CD in the absence of ADH

1) PT - isoosmotic resorption
2) descending limb - only permeable to water (concentrates urine)
3) thin ascending limb - impermeable to water, NaCl leaves urine, urea enters urine
- more NaCl leaves than urea enters - dilution
4) Thick ascending limb - impermeable to water and urea; active resorption of NaCl, urine leaving segment is hypo-osmotic with regards to plasma
5) DT and cortical CD: active resorption of NaCl, no water resorption in the absence of ADH
6) Medullary CD: active resorption of NaCl, small amount of water resorption in the absence of ADH

- in the absence of ADH, can get very dilute urine (50 in kids, 100-200 in elderly)

37

Concentrating urine

Water is never pumped, only diffuses
Kidney makes a hyperosmotic "sink" in interstitium to pull water out of urine, accomplished by thick ascending limb of LOH

1) PT to thick ascending limb: TAL extremely important in creating hyperosmotic interstitium to pull water out in medullary CD
- action of NKCC and Na/K ATPase
- countercurrent multiplication
2) DT and cortical CD: hypoosmotic filtrate
- ADH presence: presence of aquaporins - water filters out of urine
- can be concentrate to ~290 mosm/ kg water
- composition: less NaCl, more creatinine, urea, ammonia, K+
3) Medullary CD: osmolality of interstitium increases as moves down into medulla
- ADH: makes this permeable to water
- urine can be concentrated to ~1200 mosm/kg

38

Posm equation

2[Na+] + glucose + urea