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98 Cards in this Set

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  • Back
What are the major ions in the ECF?
CNBC - best news on tv
-Na - highest ~142
-Cl - second highest ~106
-Bicarb - ~24
-Ca - ~5
What are the major intracellular ions?
-K ~140
-Phosphate ~135
What happens when a person on a normal low-sodium diet suddenly increases their daily intake from 30 mEq/day to 300 mEq/day?
They retain sodium for about 2 days before excretion once again equals the new high intake.
Where is sodium distributed in the body?
In the ECF
If we're retaining sodium what do we also know must be happening? Why?
We must be retaining water - to maintain the same ECF osmolarity.
How do we know that we're retaining water if we're retaining sodium?
Because of the graph that says if ADH/thirst systems aren't blocked, plasma Na conc will stay THE SAME.
Does the kidney instantly decrease its excretion rate if sodium intake goes back down to 30 after the jump to 300 mEq/day?
No; it's a stepwise decrease and kidney excretion rate remains elevated a couple of days as the excess sodium is lost.
What happens to the ECF when sodium intake jumps to 300 mEq/Day?
Its VOLUME increases from about 11 L to 12 L over a period of 2 days
What happens to ECF volume when sodium intake goes back down to normal?
It goes back down to 11 L over a period of about 2-3 days.
What are the basic processes that can be changed to alter the kidney's handling of sodium?
1. Filtration
2. Reabsorption
3. Secretion
What happens to sodium at the glomerulus?
It is freely filtered
What is the concentration of sodium in Bowman's space?
The same as that in the glomerular capillaries
How much sodium is absorbed in the proximal tubule?
How much sodium is absorbed in the loop of henle?
How is sodium reabsorbed in the thin loop of henle?
By passive reabsorption
How is sodium reabsorbed in the thick loop of henle?
By active reabsorption
How much sodium is reabsorbed in the distal convoluted tubule?
(early + late)
How much sodium is reabsorbed in the collecting duct?
How much sodium is excreted?
What is a change in plasma volume really?
Change in plasma sodium
What are the 3 sensors of plasma volume changes?
1. Low pressure baroreceptors
2. High pressure baroreceptors
3. Intrarenal control receptors
Where are the low pressure baroreceptors?
In the great veins and atrium
Where are the high pressure baroreceptors?
In the carotids and aortic arch
What are the intrarenal control receptors for detecting plasma volume (2)?
-Macula densa cells
-Renal Vascular receptors
Where are the macula densa cells?
In the distal tubule
What are the macula densa cells sensitive to? How do they work?
Decreasing Sodium levels - they regulate renin release.
What are the renal vascular receptors sensitive to?
Arterial pressure
How do the renal vascular receptors work?
As arterial pressure increases it increases the stretch of these receptors and alters the release of renin.
What are the 4 major components of hormonal control of Na excretion?
1. RAS
2. Aldosterone
3. Sympathetic nerves
4. ANF
What is Renin?
An enzyme
What does Renin do?
Activates Angiotensinogen to Ang I
Is Angiotensin I active?
not really
What activates Angiotensin I?
ACE in the endothelium of the lungs
What does ACE produce?
Ang II
What is Ang II?
A potent vasoconstrictor
What is the preferential site of action of Ang II?
Efferent arteriole
What kind of innervation is carried in the renal nerves?
What 3 things stimulate Renin release from juxtaglomerular cells?
1. Renal nerves (SNS)
2. Low intrarenal pressure
3. Low NaCl sensed by macula densa cells
Where are macula densa cells?
in the thick ascending tubule cells
What do the macula densa cells sense?
Decreased sodium in filtrate
3 effects of Ang II produced by Renin release:
1. Increased Aldosterone
2. Global vasoconstriction (decreased GFR)
3. Increased Na reabsorption in the proximal tubule
How does Ang II stimulate Na reabsorption in the proximal tubule?
By increasing the activity of the Na/H exchanger there.
What is the effect of increasing sodium retention?
Increased ECF
What is the effect of vasoconstriction?
Increased TPR
What is the effect of increased ECF and TPR?
Increased MAP
What 3 things does increased MAP do?
1. Increases NaCl sensed by macula densa
2. Increases intrarenal baroreceptors
3. Decreases renal symp activity
What does Ang II do under normal conditions?
Constricts the efferent arteriole
What does Ang II do at high elevated levels?
Constricts the whole renal vasculature
What does constricting just the efferent arteriole do to GFR? What about the whole vasculature?
Efferent = increased GFR

Whole vasc = decreased GFR
Where is renin released from?
Granules in the afferent arteriole
Where does Ang II stimulate increased reabsorption of Na? How?
-In the proximal tubule by stimulating Na-H exchangers
-In the distal tubule by stimulating Aldosterone release
Where is Aldosterone made and released?
In the zona glomerulosa of the adrenal gland
What is Aldo release stimulated by?
1. Increased Ang II
2. Increased plasma K
What is the effect of Aldosterone?
Increased Na reabsorption and K excretion in the principle cells of the late distal tubule and cortical collecting duct.
What are the passive sodium channels in the principle cells sensitive to?
What are the 3 ways that Aldosterone acts on principle cells?
1. Increases the conc of apical Na and K channels to increase permeability
2. Stimulates synthesis of Na/K ATPase
3. Stimulates expression of Na/K ATPase at basolateral membrane.
What stimulates the Renal Sympathetic Nerves?
Low ECF volume
Where is low ECF volume primarily sensed?
In the veins by the low pressure baroreceptors
Where else is low ECF volume sensed?
In the arterial low pressure baroreceptors when MAP is low
3 effects of Renal SNS activity on renal function:
1. Stimulates renin release
2. Stimulates proximal tubular reabsorption via Na/H exchanger
3. Vasoconstricts the renal vasculature
Where is the Na/H exchanger stimulated by the SNS nerves?
In the proximal tubule - same one as that stimulated by Ang II
What type of neurotransmitter is released by the SNS nerves?
What receptor on the renal tubular cells does norepi hit?
Alpha 1 receptors
What is ANF stimulated by?
Increased ECF volume
2 effects of ANF on renal function:
1. Decreased Na reabsorption in the collecting duct
2. Dilation of the renal vasculature
How does ANF decrease sodium reabsorption in the collecting duct?
By inhibiting the medullary ENaC channels
Where is the ANF released from?
Stretched Atria
What are the hormones most important in regulating?
Sustained changes in sodium intake
What is more important in regulating the short term response to changes in sodium intake?
Physical factors
What is the main important physical factor?
plasma protein
What will happen if you take in a lot of fluid?
It will dilute your plasma proteins
2 effects of diluted plasma proteins:
1. Increased GFR
2. Decreased Peritubular cap reabsorption
Why does dilution of plasma proteins increase the GFR?
Because there is less plasma oncotic pressure opposing filtration in the glomerulus
Why does dilution of plasma protein decrease peritubular cap reabsorption?
Because there is less oncotic pressure pulling solutes into the capillary.
2 things that can change the peritubular capillary's tendency to reabsorb:
-Hydrostatic pressure
-Oncotic pressure
3 things that increase peritubular capillary hydrostatic pressure:
-Decreased renal vascular resistance (aff/eff)
-Increased MAP
What does increased peritub cap hydrostatic pressure do to its reabsorption?
Decreases it
What 2 things change the colloid oncotic pressure in pcaps?
-Systemic plasma colloid oncotic pressure
What happens to PCap oncotic pressure if systemic oncotic pressure is increased?
Same thing; it increases
What happens to plasma colloid oncotic pressure if GFR increases?
Colloid oncotic pressure increases because its relative concentration is now higher.
What else can elevate the plasma colloid oncotic pressure?
Increased filtration coefficient
How do you increase the filtration coefficient?
By changing the permeability or surface area of the capillaries
And how does increasing pcap colloid oncotic pressure change filtration pressure?
It increases reabsorption.
What is a physiological situation in which we would see a decrease in peritubular capillary reabsorption? Why?
Taking on isotonic NaCl solution
-Increases MAP (Na trapped)
-Decreases oncotic pressure via dilution of incr ECF vol
-Renal nerve activity decreased
-RAS decreased
What is the feedback capability of the hormonal and nerve regulation of ECF vol?
What is the primary controller of ECF vol in the LONG TERM?
The renal body fluid feedback mechanism
What is the feedback capability of the renal-body fluid feedback system?
What is the basis of this system?
When MAP increases, sodium and water output will increase 2X as much to return MAP all the way back to control.
If you drink a liter of water where does it go?
To the ECF; osmolarity decreases, so water goes where the salt is - into cells.
So what expands when you drink water?
Both intracellular and extracellular water.
How does the body sense it when you drink water?
-By the decrease in osmolarity (most important)
-And the increase in volume (less important)
What would happen if you drank isotonic saline?
It would be absorbed by the gut, into gut capillaries, and stay there; no osmotic force for movement.
Where would the NaCl load distribute if you drank isotonic saline?
Into the ECF vol
What is the best way to volume load? water or isotonic saline?
Drink isotonic saline.
Why not water?
It would just go into your cells, not your ECF.
What happens if you consume copious amounts of a hypertonic NaCl load?
The gut absorbs it, gut caps absorb it, then water goes where the ions are, so cells shrink as water shifts to ECF.
What is stimulated by increased plasma osmolality?
-ADH release
So you drink some water; what happens?
-Plasma volume expands
-Plasma oncotic pressure decreases