Location Na+ reabsorb Cl- reabsorbed H2O reabsorbed K+ reabsorbed End osmolarity

(mosmol/kg H2O)
Proximal tubular 65% 65% 65% 55% 300
reabsorption

LOH Descending - none Descending – none Descending 15% Descending – secretes 100

Ascending 25% Ascending 25% Ascending – none Ascending

- 30% +
- secreted amount
Distal tubular 5% 5% None <100
reabsorption

CD 5% 5% 8-19% 0-5%
Min ADH 8% 30
Max ADH >19%
1400
Excreted in urine <1% 10-15%
Difference 1) both paracellular
& transcellular
2) CD Type B intercalated cell
- dependent on H+ ATP-ase
pump
FLUID & ELECTROLYTE BALANCE
94A3 Explain the mechanisms involved in sodium handling by the kidney

Na+ handling by the kidney 5

- All location basolateral membrane: 3Na+/2K+ ATP-ase

- Apical membrane channel differs as follows

PCT: 65% -Apical membrane:

- co-transporter: Na+-Glucose or Na+-A.A.
- counter-tranpsort: Na+/H+ channel or Na+/NH+ channel

Glomerulotubular Balance
- Na+ reabsorption by PCT is adjusted to match GFR
2 mechanism:
a) ↑ GFR  ↑ glucose and amino acid load  ↑ Na+ reabsorption
b) ↑ GFR  ↑ protein conc in capillary plasma  ↑ oncotic pressure
 ↑ solute/H2O reabsorption
Aim:
a) minimize impact of GFR change on amt of Na+ and water excretion in urine

aLOH: 25% - Apical membrane:

- NCKK co-transporter
- Na+/H+ counter-transporter

Both (dLOH and aLOH) have some passive paracellular Na+ reabsorption
due to positive luminal potential.

DCT: 5% - Apical Membrane

-Na+-Cl- co-transporter
- ENaC (epithelial Na+ Channel)
CD: 5% - Apical membrane:
(principle cell) - ENaC

Control of Na+ reabsorption/excretion in the kidney

- Normally 96% to over 99% of filtered sodium is reabsorbed.
- 1-4% excreted: depends on amount ingested
adjusted by amount filtered & amount reabsorbed.
- Most is reabsorbed with Cl -, some when H+ is secreted & a very small amount in association with K +
secretion.

REGULATIONS OF Na+ REABSORPTION

1. Glomerulotubular balance @ PCT: match GFR to Na+ reabsorption

- ↑ GFR  ↑ glu/aa filtered  ↑ Na+ reabsorption
- ↑ GFR ↓ oncotic pressure going to peritubulary capillary ↑solute & H2O reabsorption

2. Hormone:
a) Aldosterone: @ CD: ↑ Na+ reabsorption
principal cells ↑ Na+/K+ pump; ↑ ENaC; ↑ K+ channels
intercalated cells ↑ H+/K+ pump; ↑ H+ ATP-ase pump
- ↑ aldosterone by ↓ dietary salt
Any events that activate the RASS

b) Renin-Angiotensin II: ↑ Na+ reabsorption via marked ↓ GFR

i) potent vasoconstriction: both the afferent and efferent arterioles
(↓RBF)
ii) constrict messangial cells: ↓ SA (↓Kf)  ↓ GFR
iii) ↑ Na+ reabsorption in PCT, DCT, CD

iii) aldosterone release

iv) (direct hypothalamus effect: Thirst and ADH)
v) augment sympathetic activity

c) ADH ↑ Na+ reabsorption in collecting duct

d) Atrial Natriuretic Peptide: ↑ Na+ / water excretion

i) ↑ GFR by dilating afferent arteriole but constrict efferent arteriole
ii) by ↑ filtration coefficient, Kf,

iii) inhibit renin secretion

 iv) inhibit aldosterone release fr adrenal corex

v) directly inhibit Na+ reabsorption in collecting ducts (no effect on

ADH)

e) Endothelin & IL-1: ↑ PGE2 formation  natriuresis

3. Renal SNS nerves - ↑ Na+ reabsorption

i) RBF & GFR and
ii) directly stimulate Na+ reabsorption by renal tubules.

4. Pressure natriuresis & diuresis - most important controller of blood volume.

glomerular capillary hydrostatic pressure GFR (minor)
renal artery pressure peritubular capillary hydrostatic pressure   renal interstitial pressur
 Na reabsorption

5. Arterial, renal & cardiac baroreceptors indirectly GFR when body Na+ falls.

:. ↓ body Na+
 ↓ ECF
i) Direct effect: ↓ ECF  ↓ NFP (net filtration pressure) - ↓ hydrostatic pressure
- ↑ oncotic pressure
 ↓ GFR  ↓ Na+ excretion
ii) Indirect effect: ↓ ECF stimulate baroreceptors (high pressure and low pressure)
(renal JGA baroreceptors)
a) Hormones: ↑ Renin-angiotensin II
↑ Aldosterone
↑ ADH
↓ ANP
↓ pressure natriuresis and diuresis
b) ↑ SNS response

↑ body Na+  reverse is true

Chloride Handling
Same as Na+ handling, except
1) Cl- reabsorption is both paracellular and transcullular.
2) Coupled to sodium reabsorption

3) At DC, type A or B intercalated disc

a) not dependent on Na+/K+ ATP-ase pump

b) dependent on the H+ pump
:. 65% PCT
25% aLOH
5% DCT
5% CD (Type B intercalated cells)

Water Reabosrption

Reabsorption by osmosis:

PCT 65%
dLOH 15%

aLOH impermeable to H2O

DCT relatively impermeable to H2O

CD ADH increase permeability of collecting duct via aquaporins

8-19% water reabsorption

Obligatory water loss

= daily renal solute load (require excretion) = 700 mosmol = 500mls water
Max urinary concentration 1400 mmol/L

Complete absence of ADH

DI: 25-30L/day of urine produced

Control of Water reabsorption

= as for Na+ reabsorption

Primary control is at collecting ducts: ADH

- release of ADH is controlled by hypothalamus
a) baroreceptors reflex
b) osmoreceptors reflex
Potassium Reabsorption K+ Cl-
All basolateral membrane has Na+/K+ ATP-ase pump.
Cl-, K+
PCT 55% a) Basolateral membrane
(Na+/K+ ATP-ase pump)
K+-Cl- co-transport

b) Paracellular: K+ and Cl- reabsorption

aLOH 30% a) Basolateral membrane

(Na+/K+ ATP-ase pump)
K+-Cl- co-transport

b) Apical membrane
NKCC co-transport
K+ channel (K+ to tubular fluid)

CD 0-5%
i) Principal Cell a) Basolateral membrane
(Na+/K+ ATP-ase pump)
K+ channel (into peritubular capillary)

b) Apical membranee
K+ Channel (into tubular fluid)
ENaC

ii) Intercalated Cells

Type A Type B

Apical membrane: H+/K+ ATP-ase pump Basolateral membrane: H+/K+ ATP-ase pump

Excreted in urine : 10-15%

Remember:
Type A intercalated cells

Type B intercalated
cells

Secrete acids into urine

Secrete base (HCO3-)

into urine
At apical membrane

At apical membrane
- H+ ATP-ase pump

- HCO3-/Cl-
Factors affecting K+ absorption:

a) Tubular flow rate: ↑ flow rate  gradient for K+ to be secreted

b) Cells: physiological: - Aldosterone: ↑ K+ secretion

- ↑ Na+/K+ ATP-ase pump
- ↑ K+ channel

- ADH: ↓ K+ secretion

Drugs: - Loops diuretics: reduce K+ reabsorption

- Thiazide diuretics: K+ secretion as distal part reabsorb Na+,
electrical gradient generated

c) Plasma K+ ↑ plasma K+  ↑ K+ secretion

a) directly stimulate basolateral membrane of Na+/K+ ATPase pump
b) directly stimulates aldosterone release fr adrenal cortex: ↑ Na+/K+ pump
↑ K+ channel
Plasma acidosis: ↑ renal K+ reabsorption

Net effect: plasma hyperkalaemia

- H+/K+ exchanger in type A intercalated cells
 increase K+ reabsorption

- cells: high plasma hydrogen ion, K+ move out cell, H+ into cells
- Insulin/adrenaline: stimulate Na+/K+ ATP-ase: K+ into cells

Plasma alkalosis: ↑ renal K+ secretion

↓ plasma H+ ion  stimulate basolateral membrane Na+/K+ ATPase pump

Net effect plasma hypokalameia (opposite effect)

Note:

a) Body Na+ changes:

no net effect on K+
excretion

- ↑ Na+  ↑ ECF 
aldosterone inhibited ↓
K+ excretion


↑ GFR  ↑ filtrate flow  ↑
K+ excretion
b) Body water content changes:
no net effect on K+
excretion

- ↑ water  ↓ ADH
 ↓ K+ excretion

↑ GFR
 ↑ K+ excretion