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129 Cards in this Set

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Peritubular capillary hydrostatic pressure
13 mm Hg
Peritubular capillary oncotic pressure
32 mm Hg
Renal ISF hydrostatic pressure
6 mm Hg
Renal ISF oncotic pressure
15 mm Hg
Sum of forces out of peritubular capillary:
28 mm Hg
Sum of forces in at peritubular capillaries
38 mm Hg
Net filtration pressure at peritubular capillaries:
28-38 = -10 inward
Process by which substances are taken into peritubular capillaries:
Bulk flow
What is "glomerulotubular balance"?
The ability of the Tubules to increase their reabsorption rate in response to an increased tubular load.
What is the normal GFR?
125 ml/min
What is the normal absolute rate of proximal tubule reabsorption?
65%GFR = 81 ml/min
If you increase the GFR from 125 ml/min to 150 ml/min how much will the absolute rate of proximal tubule reabsorption increase?
From 81 ml/min to 97.5 ml/min -> 65% of GFR
So what happens to PT reabsorption as GFR increases?
-Absolute rate increases
-Percentage of GFR remains constant
Does glomerulotubular balance only occur in the proximal tubules?
No, also in the loops of henle and other tubular segments.
Why is glomerulotubular balance important?
It helps prevent overloading of the distal tubular segments when GFR increases.
What %age of water and solutes are reabsorbed from glomerular filtrate as it passes through the tubules?
99%
What is the normal rate of peritubular capillary reabsorption?
124 ml/min
What is the Kf of peritubular capillaries? Units? Why? (2 reasons)
12.4 ml/min/mm Hg - pretty high
-Surface area of these caps is high
-High hydraulic conductivity
What are the 2 determinants of peritubular capillary reabsorption that are directly influenced by renal hemodynamic changes?
-Peritubular cap colloid oncotic pressure
-Peritubular cap hydrostatic pressure
What is peritubular cap hydrostatic pressure under the influence of? (2 things)
1. Arterial pressure
2. Resistance in the afferent and efferent arterioles
What will increasing arterial pressure do to the pcap hydrostatic pressure and reabsorption?
Increase it - thus decreasing reabsorption.
What buffers increases in Pcap hydrostatic pressure due to increased arterial pressure?
Autoregulatory mechanisms - to some extent.
What will an increase in resistance of the afferent or efferent arteriole do to pcap hydrostatic pressure? To reabsorption?
-Decrease Pcap hydrostatic pressure
-Increase peritubular cap reabsorption
So how does constricting the efferent arteriole affect the hydrostatic pressure in:
-Glomerular capillaries
-Peritubular capillaries
Gcaps - it increases their hydrostatic pressure
Pcaps - it decreases their hydrostatic pressure
What are the 2 determinants of pcap oncotic pressure?
1. Systemic plasma colloid oncotic pressure
2. Filtration fraction
What determines systemic colloid oncotic pressure?
Plasma proteins
If pcap oncotic pressure increases, how is reabsorption affected?
It will increase
So if plasma protein concentration is increased how does it affect pcap reabsorption?
Increased
Why does the filtration fraction affect plasma oncotic pressure?
If the filtered fraction is increased, the remaining protein after the glomerulus is more concentrated, so reabsorption is higher.
What can increase the filtration fraction?
-Increased GFR
-Decreased RPF
What hormone can decrease RPF? How?
Angiotensin II - by vasoconstricting
What are the tight junctions in the proximal tubule like?
Leaky - once solutes and water have diffused or been AT'd into renal ISF they can diffuse back into the tubule cells.
What do we call it if solutes move back into tubule cells?
Backleak
How much backleak is there normally? Why?
Not much - because the peritubular capillaries have high oncotic pressure and low hydrostatic pressure, favoring reabsorption.
What happens to backleak if capillary reabsorption is decreased?
Interstitial hydrostatic pressure increases, pushing more backleak.
So peritubular capillary reabsorption is closely linked with
Tubule reabsorption; increasing one will increase the other, and vice versa.
Where exactly is the pathway for backleak?
Paracellular
How do small increases in arterial pressure affect urinary excretion?
Even small increases in arterial pressure cause marked increases in urinary excretion!
What do we call increased sodium and water excretion in response to increased arterial pressure?
-Pressure Natriuresis
-Pressure diuresis
What does an increase in arterial pressure from 75-160 mm Hg do to RBF and GFR?
Not much - GFR only increases slightly.
Why does GFR slightly increase in response to an increase in arterial pressure?
ONly because urinary excretion increases.
How does increasing MAP affect peritubular capillaries? What is the result?
It increases their hydrostatic pressure; decreasing reabsorption; increases backflow.
What does increased backflow contribute to pressure diuresis and natiuresis?
It helps them by pushing more sodium back into the filtrate.
What does increased arterial pressure do to Ang II? What is the result?
Decreases its production; less sodium/water retention, more urinary output.
Where is the site of action for Aldosterone?
Na/K ATPase on the basolateral membrane of the Late Distal tubule and Cortical Collecting Duct Principle cells
What does Aldosterone do?
Increases Na/Cl/H2O reabsorption
Increases K secretion
Where is the site of action of Ang II? (not vascular)
Proximal tubule
What does Ang II do?
Increases NaCl/H2O reabsorption
Increases H+ secretion
Where is the site of action of ADH?
Distal tubule/collecting ducts
What does ADH do?
Increases water reabsorption
Where is the site of action of ANP?
Distal tubule/collecting ducts
What does ANP do?
Decreases NaCl reabsorption
Where are the 3 sites of action of PTH?
-Proximal tubule
-Thick ascending loop of Henle
-Distal tubule
What does PTH do?
-In the prox tubule:
-In the thick asc. limb of LOH and the distal tubule:
Decreases Phosphate reabsorption in the proximal tubule
Increases Calcium reabsorption in the thick ascending LOH and Distal tubule
What cells are the target of Aldosterone?
Principle cells in the late distal tubule and cortical collecting duct.
What is the mechanism by which Aldosterone increases sodium reabsorption and K secretion?
It stimulates the Na/K pump on the basolateral membrane.
What is addison's disease?
Absence of aldosterone
What is Conn's syndrome?
Too much aldosterone
What are the 3 things Ang II does?
1. Stimulates aldosterone secretion
2. Constricts efferent arterioles
3. Stimulates sodium reabsptn at the proximal tubules
What does SNS activation do to kidney excretion?
-Constricts renal arterioles
-Reduces GFR
-Decreases Na/H2O excretion
What reabsorption is affected by SNS activity?
Sodium reabsorption is increased
What hormone is affected by SNS? How?
Renin - SNS activity stimulates its release
So SNS activity will in general do what?
Make you retain sodium and water.
Is plasma calcium freely filtered by the kidney?
No
Why isn't calcium freely filtered?
B/c 50% of it is bound to plasma proteins.
Where is Calcium reabsorbed? How much at each site?
-Proximal tubule - 67%
-Thick ascending limb of LOH 20%
-Distal tubule 9%
-Collecting duct 1%
How much calcium is excreted?
1%
By what pathways is calcium reabsorbed at the Prox Tubule?
-Paracellular
-Transcellular
How does calcium get from the prox tubule lumen into cells?
By specific 2ndary active transporters
What 2 transporters take Calcium from the PCT cells into the ISF?
-Ca/2H ATPase
-Ca/3Na Active Transporter
What happens to the lumen electrical potential at the Thick Ascending limb?
It becomes +8 mV
What does the +8 mV potential do for reabsorption in the thick ascending limb?
It DRIVES ions - Na/K, Mg, Ca - into the tubule cells via passive Paracellular Diffusion
By what mechanisms does Calcium get reabsorbed at the thick ascending limb of LOH?
BOTH paracellular and transcellular
What regulates the transcellular uptake of Calcium at the Thick Ascending limb of LOH?
PTH
By what mechanism does Ca get reabsorbed at the DISTAL tubule?
what transporter?
Transcellular only via ECaC
What regulates Ca reabsorption at the distal tubule?
PTH
What does the percentage of filtered calcium reabsorbed at each tubular segment mimic?
The same pattern of sodium.
Where does PTH regulate Calcium reabsorption?
-Thick ascending limb of LOH
-Distal tubule
What does increased PTH do to calcium reabsorption?
Increases it
What stimulates PTH increase?
Decreased plasma calcium
3 effects of increased PTH:
1. Increased Vit D3 activation
2. Increased Renal calcium reabsorption
3. Increased calcium release from bones
What does increased vit D3 activation do?
Increases intestinal calcium reabsorption.
6 changes that will DECREASE CALCIUM EXCRETION:
1. Increased PTH
2. Decreased ECF volume
3. Decreased blood pressure
4. Increased plasma phosphate
5. Metabolic acidosis
6. Vitamin D3
Is phosphate filtered freely?
No; 10% is bound to plasma proteins.
Where is Phosphate reabsorbed? How much?
Proximal tubule - 80%
Distal tubule - 10%
How much phosphate is excreted?
10%
What will affect how much you excrete phosphate?
Your dietary intake
What transporter takes Phosphate from the proximal tubule lumen into the cells?
Pi/N cotransporter - both down their gradient.
What takes phosphate out of the tubule cell into the ISF?
Pi/A- exchanger (active transport)
By what mechanism is Phosphate reabsorbed in the prox tubule?
Transcellular only
Is phosphate reabsorption in the prox tubule regulated hormonally?
Yes
What hormone regulates Pi reabsorption in the PCT, and how?
PTH - increased PTH will decrease PI reabsorption.
What will happen to phosphate handling if the plasma concentration is < 0.8 mM?
It will be completely reabsorbed
What happens if plasma phosphate levels are > 0.8 mM?
It will be excreted
What hormone regulates phosphate reabsorption in the proximal tubule?
PTH
What will increases in PTH do to phosphate reabsorption? How?
Decrease it - by inhibiting the transporter by decreasing cAMP levels.
And what is essential for Phosphate to even get from the lumen into the prox tubule cell?
Sodium! For the sodium/Pi cotransporter
5 factors that will decrease Pi excretion (increase reabsorption):
1. Decreased PTH
2. Phosphate depletion
3. Decreased ECF volume
4. Metabolic alkalosis
5. Growth hormone
5 Factors that will increase Pi excretion (decrease reabsorption):
1. PTH hormone
2. Pi loading
3. Increased ECF vol
4. Metabolic acidosis
5. Glucocorticoids
Is magnesium freely filtered at the glomerulus? Why not?
No - because 50% is bound to plasma proteins.
How much of each is bound to plasma proteins?
-Ca
-Pi
-Mg
Ca = 50%
Pi = 10%
Mg = 50%
Where is Magnesium reabsorbed, and how much at each site?
Prox tubule - 35%
Loop of Henle - 65%
What perhaps regulates Magnesium reabsorption?
Calcitonin
What are 3 things that will increase Magnesium excretion (decrease reabsorption)?
-Increased Mg in ECF
-Increased Ca in ECF
-Increased ECF vol
Is water freely filtered at the glomerulus?
Yes
Where is water reabsorbed? How much at each site?
Prox tubule - 65%
Loop of Henle - 20%
Distal tubule - 5%
Collecting duct - 9.5%
Where does ADH regulate water reabsorption?
At the late distal tubule and collecting duct.
By what mechanisms is Water reabsorbed at the Prox tubule and thin desc limb of LOH?
-Paracellular
-Transcellular
What drives water reabsorption in the proximal tubule?
Osmosis
What is the osmotic gradient across the prox tubule epithelium?
19 mOsm mm Hg -> 1 mOsm/L
Why is it that water can so easily diffuse through the prox tubule?
Because the tight junctions are leaky there.
What happens to the water permeability of tubule cells at the thick ascending limb of LOH?
They become completely nonpermeable to water.
Why does the water permeability decrease so drastically in the thick ascending limb of LOH?
Because the tight junctions have high electrical resistance.
What is the mechanism by which water is reabsorbed in the distal tubule and collecting duct?
By transcellular transport of Aquaporins only!
What controls reabsorption of water in the distal tubule and collecting duct?
ADH
What if there is no ADH?
There won't be any aquaporins inserted, so no water reabsorption.
What type of Aquaporins are regulated by ADH? Where?
AQP2 on the apical/lumenal membrane.
What type of AQPs are on the basolateral membrane? Are they regulated?
3/4 - not regulated by ADH; these are constitutive.
How much urea is:
-Filtered
-Reabsorbed
-Secreted
-Excreted
Freely filtered - 100%
Reabsorbed - 120%
Secreted - 60%
Excreted = 160-120 = 40%
Where is Urea reabsorbed?
Prox tubule - 50%
Medullary collecting duct70%
Where is urea secreted?
Thin desc or ascending limbs of LOH - 60%
What controls urea reabsorption in the inner medullary collecting duct?
ADH
So an increase in ADH will do what?
Increase water reabsorption
Increase urea reabsorption
-In the medullary collecting duct
Why is urea reabsorbed from the proximal tubule? How much?
Because a lot of other water and solutes are reabsorbed, so it follows them. 50%
What is the mechanism by which urea is reabsorbed in the prox tubule?
Passive paracellular diffusion
What type of transporters secrete Urea in the desc/asc thin limbs of henle's loop?
By what mechanism?
Active transporters - by transcellular transport only.
What type of transporters reabsorb urea in the inner medullary collecting duct? Under the control of what?
UT1 and UT4
Under the influence of ADH.
Where is UT1 found?
On the apical membrane
Where is UT4 found?
On the basal membrane.