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Tubular Reabsorption

Figure 27-1;
Guyton and Hall
Copyright2006byElsevier,Inc.

Primary Active Transport of Na+

Figure 27-2;
Guyton and Hall
Copyright2006byElsevier,Inc.

Mechanismsof
Secondary
ActiveTransport

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Figure 27-3;
Guyton and Hall

GlucoseTransport
Maximum

Figure 27-4;
Guyton and Hall
Copyright2006byElsevier,Inc.

Reasorption of Water and Solutes is


Coupled to Na+ Reabsorption
Tubular
Cells

Interstitial
Fluid

- 70 mV
Na +

K+

ATP

Na +
ATP

0 mv
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K+

Tubular
Lumen

H+
Na +
glucose, amino
acids
Na +
Urea
H20
Na +

Cl-

- 3 mV

MechanismsbywhichWater,Chloride,
andUreaReabsorptionareCoupledwith
SodiumReabsorption

Figure 27-5;
Guyton and Hall
Copyright2006byElsevier,Inc.

CellularUltrastructureandPrimary
TransportCharacteristicsofProximal
Tubule

Figure 27-6; Guyton and Hall


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CellularUltrastructureandTransport
CharacteristicsofThinandThickLoop
ofHenle
very permeable
to H2O)

not permeable
to H2O)
Figure 27-8;
Guyton and Hall
Copyright2006byElsevier,Inc.

SodiumChlorideandPotassiumTransportin
ThickAscendingLoopofHenle

Figure 27-9;
Guyton and Hall
Copyright2006byElsevier,Inc.

CountercurrentMultiplierSystem
intheLoopofHenle

Figure 28-3; Guyton and Hall

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Countercurrentmultiplieranimation

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RecirculationofUreaAbsorbedfromMedullary
CollectingDuctintoInterstitialFluid

Figure 28-5; Guyton and Hall


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NetEffectsof
CountercurrentMultiplier
1. More solute than water is added to the renal medulla
(i.e., solutes are trapped in the renal medulla).
2. Fluid in the ascending loop is diluted.
3. Horizontal gradient of solute concentration established
by the active pumping of NaCl is multiplied by
countercurrent flow of fluid.

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TheVasaRectaPreserve
HyperosmolarityofRenalMedulla
The vasa recta
serve as
countercurrent
exchangers
Vasa recta blood
flow is low
(only 1-2 % of
total renal
blood flow)

Figure 28-3; Guyton and Hall


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SodiumChlorideTransportin
EarlyDistalTubule

Figure 27-10;
Guyton and Hall
Copyright2006byElsevier,Inc.

CellularUltrastructureandTransport
CharacteristicsofEarlyandLateDistalTubules
andCollectingTubules
not permeable
to H2O
not very
permeable to
urea

permeability
to H2O
depends on ADH
not very
permeable to
urea
Figure 27-11; Guyton and Hall

Copyright2006byElsevier,Inc.

SodiumChlorideReabsorptionandPotassium
SecretioninCollectingTubulePrincipalCells

Figure 27-12;
Guyton and Hall
Copyright2006byElsevier,Inc.

Cortical Collecting Tubules


Intercalated Cells
Tubular Cells

Tubular Lumen

H20 (depends on
ADH)
K

K+

ATP
ATP

ATP
ATP

Na +

H+
ATP

Cl Copyright2006byElsevier,Inc.

H+

CellularUltrastructureandTransport
CharacteristicsofMedullaryCollectingTubules

Figure 27-13; Guyton and Hall


Copyright2006byElsevier,Inc.

Normal Renal Tubular Na+ Reabsorption


7%

(16,614 mEq/day)
25,560
mEq/d

(1789 mEq/d)

65 %
25 %
(6390

mEq/d)

2.4%

(617 mEq/day)

0.6 %
(150 mEq/day)
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Summary of Water Reabsorption and


Osmolarity in Different Parts of the Tubule
Proximal Tubule: 65% reabsorption, isosmotic
Desc. loop: 15-20% reabsorption, osmolarity increases
Asc. loop: 0% reabsorption, osmolarity decreases
Early distal: 0% reabsorption, osmolarity decreases
Late distal and coll. tubules: ADH dependent
water reabsorption and tubular osmolarity
Medullary coll. ducts: ADH dependent water
reabsorption and tubular osmolarity

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Concentration and
Dilution of the Urine
Maximal urine concentration
= 1200 - 1400 mOsm / L
(specific gravity ~ 1.030)
Minimal urine concentration
= 50 - 70 mOsm / L
(specific gravity ~ 1.003)

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ObligatoryUrineVolume
The minimum urine volume in which the excreted
solute can be dissolved and excreted.
Example:
If the max. urine osmolarity is 1200 mOsm/L,
and 600 mOsm of solute must be excreted each
day to maintain electrolyte balance, the
obligatory urine volume is:
600 mOsm/d
1200 mOsm/L
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= 0.5 L/day

MaximumUrineConcentrationof
DifferentAnimals
Animal

Max. Urine Conc. (mOsm /L)

Beaver
500
Pig
1,100
Human
1,400
Dog
2,400
White Rat
3,000
Kangaroo Mouse
6,000
Australian Hopping Mouse10,000

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Late Distal, Cortical and Medullary


Collecting Tubules
Principal Cells

Tubular Lumen

H20 (w/o ADH)


K+

ATP

Na +

Na +

K+
Cl -

Aldosterone
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Abnormal Aldosterone Production


Excess aldosterone - Conns syndrome
Na+ retention, hypokalemia, alkalosis,
hypertension
Aldosterone deficiency - Addisons disease
Na+ wasting, hyperkalemia, hypotension,
death if untreated
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Ang II Increases Tubular Na+ Transport


Tubular
Cells

Interstitial
Fluid

Tubular
Lumen

Ang II

Ang II
Na+

Na+

ATP

K+

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H+

Effect of Angiotensin II on
Peritubular Capillary Dynamics
Glomerular
Capillary

Ra

Peritubular
Re Capillary

Arterial
Pressure
Ang II

Re

Pc (peritubular cap. press.)


renal blood flow

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FF

Ang II Constriction of Efferent Arterioles Causes Na+


Retention and Maintains Excretion of Waste Products
Na+ depletion
Ang II
Resistance efferent arterioles
Glom. cap. press
Prevents decrease
in GFR and
retention of
waste products
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Renal blood flow

Peritub. Cap. Press.

Filt. Fraction
Na+ and H2O Reabs.

AngiotensinIIBlockadeDecreasesNa+
ReabsorptionandBloodPressure

ACE inhibitors (captopril, benazipril, ramipril)


Ang II antagonists (losartan, candesartin, irbesartan)
decrease aldosterone
directly inhibit Na+ reabsorption
decrease efferent arteriolar resistance

Natriuresis and Diuresis +


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Blood Pressure

FormationofaDiluteUrine
Continue electrolyte
reabsorption
Decrease water
reabsorption
Mechanism:
decreased ADH
release and reduced
water permeability
in distal and
collecting tubules
Figure 28-1; Guyton and Hall

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Formation of a Concentrated Urine


Continue electrolyte reabsorption
Increase water reabsorption
Mechanism:
Increased ADH release which increases water
permeability in distal and collecting tubules
High osmolarity of renal medulla
Countercurrent flow of tubular fluid

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FormationofaConcentratedUrinewhen
AntidiureticHormone(ADH)LevelsareHigh

Figure 28-4; Guyton and Hall


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Osmoreceptor
antidiuretichormone(ADH)
feedbackmechanismfor
regulatingextracellular
fluidosmolarity

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Figure 28-8;
Guyton and Hall

ADHsynthesisinthe
neuronsofhypothalamus,
releasebytheposterior
pituitary,andactionon
thekidneys

Copyright2006byElsevier,Inc.

Figure 28-9;
Guyton and Hall

Factors that Decrease


ADH Secretion
Decreased osmolarity
Increased blood volume (cardiopulmonary reflexes)
Increased blood pressure (arterial baroreceptors)
Other factors:
- alcohol
- haloperidol (antipsychotic, tics,Tourettes)

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Stimuli for Thirst


Increased osmolarity
Decreased blood volume
(cardiopulmonary reflexes)
Decreased blood pressure
(arterial baroreceptors)
Increased angiotensin II
Other stimuli:
- dryness of mouth
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Factors that Decrease Thirst


Decreased osmolarity
Increased blood volume
(cardiopulmonary reflexes)

Increased blood pressure


(arterial baroreceptors)

Decreased angiotensin II
Other stimuli:
-Gastric distention

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AtrialNatriureticPeptide(ANP)
Blood volume
ANP
Renin release

aldosterone

GFR

Ang II
Renal Na+ and H2O reabsorption
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Na+ and H2O excretion

Late Distal and Collecting Tubules


Tubular Cells

Tubular Lumen

H20 (depends
on ADH)
Aquaporin-3
H20
Aquaporins
ADH

cAMP
V2 receptor

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Vesicle

Aquaporin-2
H20

SodiumChlorideandPotassiumTransportin
ThickAscendingLoopofHenle

Figure 27-9;
Guyton and Hall
Copyright2006byElsevier,Inc.

SodiumChlorideTransportin
EarlyDistalTubule

Figure 27-10;
Guyton and Hall
Copyright2006byElsevier,Inc.

SodiumChlorideReabsorptionandPotassium
SecretioninCollectingTubulePrincipalCells

Figure 27-12;
Guyton and Hall
Copyright2006byElsevier,Inc.

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