Physiology Flashcards
(66 cards)
1
Q
Which three hormones do the kidneys secrete?
A
- kidneys secrete renin (from the juxtaglomerular apparatus) and erythropoietin
- they also activate vitamin D via 1-alpha-hydroxylase, so they technically secrete 1,25-dihydroxycholecalciferol (active vitamin D)
2
Q
If you are stranded with no water, why do you dehydrate? (ie, why don’t the kidneys just retain all the remaining water you need to survive?)
A
- the kidneys require about 500 mL of water to cleanse the body of toxic wastes and other harmful products
- they will use this amount of water even if you don’t have enough to spare! –> a person without water will eventually urinate himself to death!
3
Q
What percent of the body’s total water is in the ICF? What about the ECF? How much of a person’s body weight is water?
A
- 2/3 of H2O found in ICF; 1/3 found in ECF
- 60% of body weight is water (this means that 40% of your body weight is ICF and 20% is ECF; this is the “60-40-20 rule”)
4
Q
What are the two compartments of the ECF? Where is each found and what percent of the ECF does each make up?
A
- (remember that ECF contains 1/3 of the body’s total water)
- 2 compartments: interstitial fluid (bathes the cells) and plasma (in the blood vessels)
- interstitial fluid makes up 75% of the ECF!
- plasma makes up 25% of the ECF
- the two are essentially the same, but plasma has proteins and blood cells
5
Q
What is isosmotic volume contraction? Hyperosmotic volume contraction? Hyposmotic volume contraction? Give a major example of each.
A
- (normal osmolarity is 300 mOsm/L)
- isosmotic contraction: drop in ECF volume with no fluid shift; diarrhea (large loss of fluid via GIT results in a loss of isosmotic fluid from the ECF)
- hyperosmotic contraction: drop in ECF volume with fluid shift from ICF into ECF because of increased osmolarity; dehydration (sweating, secretions, urination result in loss of hyposmotic fluid, so you lose more water than solute)
- hyposmotic contraction: drop in ECF volume with fluid shift from ECF into ICF because of decreased osmolarity; adrenal insufficiency (no aldosterone leads to excess NaCl excretion, meaning we lose more solute than water)
6
Q
What is isosmotic volume expansion? Hyperosmotic volume expansion? Hyposmotic volume expansion? Give a major example of each.
A
- (normal osmolarity is 300 mOsm/L)
- isosmotic expansion: rise in ECF volume with no fluid shift; isotonic NaCl infusion (gain of isosmotic fluid)
- hyperosmotic expansion: rise in ECF volume with fluid shift from ICF into ECF because of increased osmolarity; very high NaCl intake (gaining more solute than water)
- hyposmotic expansion: rise in ECF volume with fluid shift from ECF into ICF because of decreased osmolarity; SIADH (gaining more water than solute)
7
Q
What is the path urine takes from its formation to its excretion?
A
- formed in kidney –> drained into renal pelvis –> channeled into ureter –> carried to urinary bladder –> emptied from the body via the urethra
8
Q
Which structures of the urinary system are lined with smooth muscle?
A
- only the ureters and the urinary bladder
9
Q
How many nephrons does each kidney have? What two regions do they form? Describe the appearance of each region. What are the two types of nephrons?
A
- each kidney has about 1 million nephrons
- they are arranged into the renal cortex and the renal medulla
- cortex = granular; lighter
- medulla = striated triangles (called “renal pyramids”); darker
- 2 types: cortical nephrons (80%) and juxtamedullary nephrons (20%); named based on the location of the glomeruli:
- the glomeruli in cortical nephrons lie in the outer layer of the cortex
- the glomeruli in juxtamedullary nephrons lie in the inner layer of the cortex, next to the medulla
10
Q
How many components are renal nephrons made up of? What are they?
A
- 2 components: vascular and tubular
- vascular component: houses the afferent arteriole, glomerulus, efferent arteriole, peritubular capillaries, and venule
- tubular component: a single hollow, fluid-filled tube with the following regions: Bowman’s capsule, proximal convoluted, proximal straight, loop of Henle (thin descending, thin ascending, thick ascending), juxtaglomerular apparatus*, distal convoluted, cortical collecting duct, medullary collecting duct, renal pelvis
- *the juxtaglomerular apparatus contains elements of both the vascular and tubular components
11
Q
What is the glomerulus?
A
- a tuft of capillaries that filters the blood passing through
- the filtrate passes through the glomerulus and into the Bowman’s capsule
- each glomerulus is supported by one afferent arteriole
12
Q
Describe the path blood entering the renal artery takes.
A
- blood enters through the renal artery –> branches into the afferent arterioles –> branches again and flows through the glomerulus –> branches join into the efferent arterioles –> branches AGAIN into the peritubular capillaries –> branches join into venules –> venules join into the renal vein
13
Q
T or F: nephrons use the glomerulus as both the filtration system and as their own blood supply.
A
- false!
- the glomerulus does NOT participate in gas exchange; it is solely for filtration
- the 2nd bed of capillaries (peritubular capillaries) is where gas exchange for the kidneys takes place
14
Q
What region(s) does the loop of Henle lie within?
A
- both the cortex and medulla; the loop begins and ends in the cortex, but dips into the medulla
- all other parts of the nephron reside in the cortex
- in cortical nephrons, the loop dips slightly into the medulla, while in juxtamedullary nephrons, the loop plunges through the entire medulla
15
Q
What is the renal clearance of albumin? What about of glucose? The clearance of what substance reflects the GFR? Why?
A
- renal clearance of albumin is zero because albumin is not filtered (because of its negative charge)
- renal clearance of glucose is also zero because, although it is filtered, it is completely reabsorbed
- inulin clearance reflects GFR (inulin is freely filtered and is neither secreted not reabsorbed); inulin is exogenous, however, the closest endogenous substance is creatinine (it is slightly secreted)
16
Q
What percent of cardiac output goes to the kidneys? At what blood pressure with GFR start to drop? How is renal blood flow regulated - which arterioles have more alpha1 receptors, which mainly respond to angiotensin II, which respond to prostaglandins?
A
- 25% of CO goes to kidneys
- GFR will start to drop once the BP is less than 80 mmHg
- afferent arterioles have more alpha1 receptors (vasoconstriction) than efferent arterioles, so sympathetic stimulation decreases GFR
- angiotensin II (vasoconstrictor) mainly acts on the efferent arterioles, so it increases GFR; ACE inhibitors/ARBs therefore decrease GFR
- prostaglandins (vasodilator) act on both arterioles and act to increase GFR; NSAIDs therefore decrease GFR
- (constricting the afferent arteriole decreases hydrostatic pressure of the glomerulus; constricting the efferent arteriole raises it)
17
Q
What are the peritubular capillaries of the juxtamedullary nephrons known as? What important process do they contribute to?
A
- vasa recta
- important in concentrating urine
18
Q
What are the three renal processes?
A
- glomerular filtration, tubular reabsorption, and tubular secretion
- filtration via the glomerular capillaries
- reabsorption and secretion occur through the peritubular capillaries
- reabsorb: Na+, Cl-, HCO3-, H2O, glucose, amino acids, urea, Ca2+, Mg2+, phosphate, lactate, citrate
- secrete: organic acids and bases, K+, H+
19
Q
What percentage of plasma entering the glomerulus is actually filtered? What equation is used to calculate GFR? What is the normal GFR?
A
- only 20% of the renal perfusion is filtered
- the remaining 80% continues into the efferent arteriole and enters the peritubular capillaries
- GFR: net filtration pressure x Kf
- (net filtration pressure is about 10, Kf is filtration constant based on surface area and permeability)
- normal GFR: 180 L/day
20
Q
What characteristics of the glomerular capillaries are essential for the high filtrative capabilities of the kidneys while also being selective?
A
- glomerulus has 3 layers: endothelial layer, basement membrane (acellular, gelatinous), epithelial layer
- the endothelial layer has very large pores/fenestrations (faster filtration because of increased permeability)
- the basement membrane contains glycoproteins with a negative charge and prevents filtration of plasma proteins by filtering based on charge (mainly albumin)
- the epithelial layer has podocytes with foot processes and filtration slits (filters based on size)
21
Q
Which forces are involved in filtration? Which ones favor it? Which ones oppose it?
A
- glomerular capillary hydrostatic pressure: 55 mmHg favoring
- plasma-colloid oncotic pressure: 30 mmHg opposing
- Bowman’s capsule hydrostatic pressure: 15 mmHg opposing
- Bowman’s capsule oncotic pressure: 0 mmHg (because no protein is filtered through the glomerulus!)
- (thus the net filtration pressure is +10 mmHg)
22
Q
Severely burned patients lose a large quantity of protein-rich plasma fluid through the exposed surface of their burned skin. What can this do to the GFR?
A
- increase the GFR
- the loss of plasma proteins results in a decreased plasma-colloid osmotic pressure, causing an increase in GFR
23
Q
How can a urinary tract obstruction (such as a kidney stone or BPH) affect GFR?
A
- the obstruction results in the damming of fluid behind the obstruction, backing up the tubular system and greatly increasing the Bowman’s capsule hydrostatic pressure
- this will cause a decrease in GFR
24
Q
Autoregulation of renal vasculature is a result of which two intrarenal mechanisms?
A
- the myogenic mechanism and the tubuloglomerular feedback (TGF) mechanism; these affect the afferent arteriole
- myogenic: automatic constriction with high pressure, dilation with low pressure
- TGF: macula dense releases ATP and adenosine in response to high Na+, causing the afferent arteriole to contract; may also secrete NO in response to low Na+
25
Apart from autoregulation and extrinsic sympathetic control, how else can the GFR be changed? What cells are involved in this mechanism?
- the filtration coefficient (Kf)
- the glomerular membrane can contract, closing off portions of the filtering capillaries, thus decreasing glomerular surface area
- these specialized cells that can contract to decrease the Kf are called mesangial cells
26
Of the average GFR (125 mL/min), how much is reabsorbed by tubular reabsorption?
- nearly all of it!
| - 124 mL/min
27
Na+ reabsorption involves what kind of mechanism? Where is Na+ reabsorbed? What percent is reabsorbed in each location?
- Na+ reabsorption relies on an active basolateral Na+-K+ ATPase pump
- is absorbed nearly throughout the entire tubule; nearly 100% of filtered sodium is reabsorbed
- 67% occurs in proximal convoluted tubule (important for secondary active reabsorption of other substances and for ECF volume maintenance)
- 25% occurs in thick ascending limb of loop of Henle* (H2O is NOT reabsorbed with it here; important for ability to concentrate urine)
- 5% occurs in the early distal tubule (also impermeable to H2O)
- 3% occurs in the late distal tubule and collecting ducts, collectively (the only percent that is regulated)
- *the only part of the tubule where Na+ doesn't occur is in the descending limb of the loop of Henle
28
The late distal tubule and collecting ducts are under what type of control for Na+ reabsorption?
- (these reabsorb 3% of Na+)
- hormonal control via aldosterone
- they are the only portions that regulate Na+ reabsorption (the rest of the tubule will always reabsorb Na+), so they are essential in fine-tuning the Na+ status
29
What substances are coupled with Na+ reabsorption in the early proximal convoluted tubule? What about in the late proximal convoluted tubule? Which substances are secreted?
- early: reabsorption of HCO3-, glucose, amino acids, (also phosphate, lactate, citrate); these are all via secondary active transport
- late: reabsorption of Cl-; via passive transport
- both secrete H+ via secondary active counter transport
- (this is where osmotic diuretics work)
- (H2O is also obviously reabsorbed here)
30
What transporter is found on the luminal membrane of the cells making up the loop of Henle? Does this transporter function from passive or active transport?
- the Na+-K+-2Cl- cotransporter (all 3 enter the cell)
- driven by secondary active transport (like all other cells, Na+ is pumped out of the cell on the basolateral side)
- remember the descending limb is impermeable to H2O
- (furosemide and other loop diuretics inhibit this cotransporter)
31
What transporter is found on the luminal membrane of the cells making up the early distal tubule? Does this transporter function from passive or active transport?
- Na+-Cl- cotransporter
- driven by secondary active transport (like all other cells, Na+ is pumped out of the cell on the basolateral side)
- impermeable to H2O
- (thiazide diuretics inhibit this cotransporter)
32
What are the two cell types present in the late distal tubule and the collecting ducts? What role does each play?
- principal cells and alpha-intercalated cells
- principal cells: reabsorb Na+, secrete K+; site of action of aldosterone (fine-tunes Na+ reabsorption and K+ secretion by regulating number of ENaC channels, luminal K+ channels, and Na+-K+-ATPase pumps) and vasopressin/ADH (regulation of H2O reabsorption)
- (ENaC channels are inhibited by spironolactone and other K+ sparing diuretics)
- alpha-intercalated cells: involved with acid-base balance (secrete H+ and reabsorb/synthesize HCO3-), reabsorb K+ via primary active transport (luminal H+-K+-ATPase pumps out H+ and pumps in K+)
33
Which substances are passively reabsorbed? How is this accomplished?
- Cl-: passively reabsorbed in the late proximal convoluted tubule via a luminal chloride-anion exchanger that is driven by the chloride gradient (additionally, Na+ active reabsorption provides a favorable electrical gradient for chloride as well)
- H2O: will follow osmotically active substances (sodium, glucose, BUN)
- urea: concentration increases as H2O is reabsorbed; 50% is reabsorbed in the proximal tubule; we don't want to reabsorb urea (but it is small enough to be absorbed), so it is also secreted in large amounts in the thin descending limb of loop of Henle, putting its concentration all the way up to 110%
34
How is glucose normally reabsorbed? What is the normal concentration of glucose in the plasma? At what concentration will glucose start to appear in the urine?
- glucose is reabsorbed in the proximal convoluted tubule
- it is reabsorbed via Na+-glucose cotransporters (SGLTs) that are driven by secondary active transport
- at the basolateral membrane, the glucose diffuses out of the cell into the interstitial fluid (and eventually to the plasma) via GLUT-1 and GLUT-2 transporters
- normal concentration of glucose is between 70 and 100 mg/dL, and normally 100% is reabsorbed
- at a concentration of 200 mg/dL, glucose will start to appear in the urine; reabsorption reaches it's maximum (tubular maximum) at a concentration of 350 mg/dL
35
What is ANP? Where and when is it produced/secreted? What does it act to do?
- atrial natriuretic peptide
- produced in the atria in response to HIGH BP
- inhibits Na+ reabsorption in the late distal tubule and collecting ducts to promote diuresis
- (also increases GFR by dilating the afferent arteriole and constricting the efferent; more salt is filtered, meaning that more will be excreted)
36
What is a filtered load? How do we calculate it? What is a tubular maximum? What is the renal threshold?
- the filtered load of a substance
- equals the plasma concentration of the substance x GFR
- tubular maximum (Tm) is the maximum rate of reabsorption of a substance (only applies to actively reabsorbed substances; note that Na+ is an exception because its reabsorption can be increased by aldosterone)
- renal threshold is the plasma concentration of a substance at which the Tm is reached (it is the plasma concentration at which a substance will start to appear in the urine)
- so long as the filtered load is less than the tubular maximum, the kidneys will reabsorb all of that substance
37
What percentage of H2O is reabsorbed at the proximal tubule? The loop of Henle? The late distal tubule and collecting ducts?
- 65% is ALWAYS reabsorbed at the proximal tubule
- 15% ALWAYS at the descending limb of the loop of Henle
- (ascending limb and early distal tubule are impermeable to H2O)
- 20% VARIABLY reabsorbed at the late distal tubule and collecting ducts (amount reabsorbed here is based on hydration status and regulated by ADH/vasopressin)
38
What are the four aquaporins? Where is each found?
- AQP-1: always inserted; found in the proximal tubule and the descending limb of the loop of Henle
- AQP-2: only inserted in presence of ADH/vasopressin; found in the late distal tubule and collecting ducts (luminal membrane)
- AQP-3 and AQP-4: always inserted; found in the late distal tubule and collecting ducts (basolateral membrane)
- (no AQPs in ascending limb of loop of Henle or in the early distal tubule)
39
What are the most important substances secreted in tubular secretion?
- H+, K+, organic cations, organic anions
| - (most organic cations and anions are foreign compounds)
40
Where is K+ reabsorbed? Where is it secreted? How is each process carried out?
- reabsorbed in the proximal tubule (secondary active transport with Na+)
- secreted in the late distal tubule and collecting ducts (passive K+ channels are located in the luminal membrane); regulated by aldosterone (increases number of Na+-K+-ATPase pumps)
41
What triggers the adrenal cortex to release aldosterone? What triggers the juxtaglomerular apparatus to release renin?
- elevated [K+] in plasma and BP trigger aldosterone release
| - decreased [Na+] in the tubule as sensed by the macula densa triggers renin release
42
What portions of the tubule secrete organic cations and anions? The kidneys can only secrete organic substances in an ionic form - what about the organic substances that are not ionic?
- the PROXIMAL tubule
- the organic substances that are not ionized are metabolized by the liver into an ionic form, allowing for tubular secretion
43
Why does the risk for drug toxicity increase if you give a patient two drugs that are both broken into organic cations or both broken into organic anions?
- because there is only one carrier for all organic cations and only one carrier for all organic anions
- if both drugs are cations/anions, the tubular secretion of each will be reduced (because of competition), the plasma concentrations of each will be increased, and toxicity can occur
44
Given that the average GFR is 125 mL/min and average reabsorption is 124 mL/min, how much urine is formed on average by the kidneys?
- 1 mL/min
45
The volume of plasma completely cleared of a substance by the kidneys per minute is known as:
- plasma clearance
| - *note that is is the VOLUME of PLASMA that is CLEARED; it is NOT the amount of a substance cleared
46
The body's interstitial fluid has an osmolarity of 300 mOsm; why then doesn't H2O reabsorption in the kidneys stop once the osmolarity of the tubule lumen hits 300 mOsm?
- because the osmolarity of the interstitial fluid of the kidneys is NOT equal to that of normal cells; there is an osmotic gradient located in the renal medulla's interstitial fluid that allows for a greater amount of H2O to be reabsorbed
- the cortex is 300 mOsm (the same as normal interstitial fluid)
- the medulla has the osmotic gradient which ranges from 600 mOsm (at the top) to 1200 mOsm (at the bottom)
- this gradient is a result of the medullary countercurrent system generated by the juxtamedullary nephrons
47
The proximal tubule always reabsorbs 65% of H2O from the filtrate before the osmolarity between the tubular lumen and the interstitial fluid equilibrates, making the remaining 35% isotonic; however, we know that another 15% is always reabsorbed by the loop of Henle - how does this occur?
- the differences between the descending and ascending limbs of the loop of Henle (of juxtaglomerular nephrons) create a countercurrent flow, which creates an osmotic gradient that favors even more reabsorption of H2O
- the descending limb is highly permeable to H2O, but does NOT reabsorb Na+ (so it doesn't transport Na+ into the interstitial fluid)
- the ascending limb is IMpermeable to H2O, but can reabsorb Na+ (so it transports Na+ into the interstitial fluid)
48
The osmolarity of the interstitial fluid is increased by the _________ limb and equilibrates with the __________ limb.
- interstitial fluid osmolarity is increased by the ASCENDING limb (Na+ is pumped out of the ascending limb and into the interstitial fluid; i.e. it is reabsorbed); filtrate osmolarity is decreasing here
- it then equilibrates with the DESCENDING limb (H2O in the descending limb diffuses into the interstitial space until equilibrium is reached); filtrate osmolarity is increasing here
49
What are the two effects of ADH/vasopressin? Which receptors correlate to which effects?
- two effects: increasing H2O reabsorption in the late distal tubule and collecting ducts, and constricting vascular smooth muscle (vasoconstriction); both lead to increased BP
- V1-receptors induce the vasoconstriction
- V2-receptors induce the insertion of AQP-2 into the membrane of the tubules
50
Explain why the maximum urine concentration that can be generated is 1200 mOsm. What does this require to be present?
- the max is 1200 mOsm because this is the highest osmolarity created in the interstitial fluid by countercurrent multiplication; once the filtrate's (urine's) osmolarity reaches 1200, it is in equilibrium with the highest osmolarity, so it can't get any more concentrated
- this requires vasopressin/ADH
51
Explain why the minimum urine concentration that can be generated is 100 mOsm.
- the min is 100 mOsm because this is the lowest osmolarity the filtrate (urine) can reach; it occurs as it enters the distal tubule; because the ascending limb of the loop of Henle is only permeable to Na+ and not H2O, the filtrate's osmolarity will decrease as it moves up this limb, reaching a minimum of 100 as it hits the distal tubule
- when vasopressin/ADH is not present, the late distal tubule and collecting ducts are impermeable to H2O, and so there is no way for H2O to be reabsorbed, and so the urine is diluted
52
The vasa recta loops into and out of the medulla; what would happen to the osmotic gradient if the blood supply (vasa recta) simply entered the medulla and flowed straight through it until it joined up with the renal vein?
- as the blood flows down the medulla (crossing through the osmotic gradient), it would continuously pick up Na+ and drop off H2O to equilibrate with the increasing osmolarity of the interstitial fluid, disrupting the gradient
- the blood supply would become extremely hypertonic (remember, 1200 mOsm!) before entering the renal vein
- the process of preserving the gradient is known as countercurrent exchange
53
What is osmotic diuresis? When is this type of diuresis classically seen?
- the increased excretion of both H2O and solute, resulting from a failure to reabsorb the solute (H2O follows the solute)
- remember that H2O always follows solute when possible, so any solute remaining in the lumen will "force" H2O to stay in as well (and be excreted in urine)
- seen in diabetes
54
What is water diuresis? When does this type of diuresis occur?
- the increased excretion of only H2O
- this will cause the osmolarity of a fluid to change (while osmotic diuresis maintains a fluid's osmolarity)
- the H2O reabsorption in the distal and collecting tubules alter the amount of water diuresis occurring to adjust the osmolarity of body fluids
- occurs with alcohol consumption
55
How is acidosis (especially respiratory acidosis) dealt with by the kidneys?
- alpha-intercalated cells in the late distal and collecting tubules take up excess CO2 present in the blood; once inside these cells, CO2 is converted into H+ and HCO3- via carbonic anhydrase
- the H+ is secreted into the lumen for excretion and the HCO3- is reabsorbed back into the blood
- thus "new HCO3-" is made
56
What path does blood take to get from the renal artery to the afferent arteriole?
- renal artery --> interlobar arteries --> arcuate arteries --> interlobular arteries --> afferent arterioles
57
What are the three components of the glomerular basement membrane? What is found in each?
- lamina rara interna (adjacent to endothelial cells): heparan sulfate proteoglycans (negative charge)
- lamina densa: type IV collagen + laminin
- lamina rara externa (adjacent to epithelial cells/podocytes): heparan sulfate proteoglycans (negative charge)
58
Why is the concentration of albumin entering the efferent arteriole greater than normal arterial blood? What equilibrates the concentration levels? Why is this important?
- the albumin concentration is greater because of the H2O that was filtered out
- this higher concentration results in a stronger colloid osmotic pressure in the blood vessels, favoring the reabsorption of H2O and equilibrating the concentration to that of normal arterial blood
- this is important because w/o the increase in reabsorption, the volume of urine output would be extremely large
59
Renal failure will lead to decreased excretion of phosphate (among other things), resulting in increased PTH secretion. Explain.
- the build-up of phosphate will result in a subsequent drop in Ca2+ because the PO4- binds to the free-floating Ca2+
- the resulting drop in Ca2+ is compensated for by the increased excretion of PTH
60
alpha-Intercalated Cells and beta-Intercalated Cells
- alpha: secrete H+ and reabsorb HCO3-; ALPHA gets activated during ACIDOSIS
- beta: secrete HCO3- and reabsorb H+; BETA gets activated when BASIC
61
What percent of K+ is in the ICF? What factors can trigger a shift from ICF into ECF (hyperkalemia)? What can trigger a shift from ECH into ICF (hypokalemia)?
- 98% of K+ is found in the ICF (only 2% is in ECF!); this is maintained by the Na+-K+-ATPase pump (pumps in K+ and pumps out Na+)
- hyperkalemia: insulin deficiency/resistance, beta2-antagonists, alpha-agonists, acidosis, cell lysis, exercise
- hypokalemia: insulin*, beta2-agonists, alpha-antagonists, alkalosis
- *insulin increases Na+-K+-ATPase pump activity
62
Where is filtered K+ reabsorbed? Where is the reabsorption regulated? Where is K+ secreted?
- 67% is always reabsorbed in the proximal convoluted tubule (follows water)
- 20% is always reabsorbed in the thick ascending limb via the Na+-K+-2Cl- cotransporter
- the late distal tubule and collecting ducts have a variable amount of K+ reabsorption/secretion based on the body's aldosterone levels and acid base status; principal cells secrete K+ and alpha-intercalated cells reabsorb K+
63
What are the major roles of phosphate? What percentage is in bone? ICF? ECF?
- phosphate has 2 major roles: a bone constituent and a urinary buffer for fixed H+ (to form titratable acid)
- 85% of phosphate is in the bone, and the remaining 15% is essentially in the ICF (as DNA, ATP, etc.); less than 0.5% is in the ECF (this is the buffering portion)
64
How much of the filtered phosphate is reabsorbed? Where does the reabsorption take place? Is it regulated by anything?
- 85% is reabsorbed (all in the proximal tubule: 70% in the proximal convoluted tubule, 15% in the proximal straight tubule)
- this means 15% is excreted; this is quite a bit! this is because phosphate is a major urinary buffer of H+ (forms titratable acid)
- its reabsorption is INHIBITED by PTH, which inhibits the Na+-phosphate cotransporter (so PTH increases phosphate SECRETION)
65
Where is calcium found in the body? How much of the filtered calcium is reabsorbed? Where does the reabsorption take place? Is it regulated by anything?
- 99% of calcium is found in the bone; the remaining 1% is split between the ICF and the ECF
- 99% is reabsorbed (67% in the proximal tubule, 25% in the thick ascending limb of loop of Henle, up to 8% in the distal tubule)
- only the distal tubule's reabsorption is regulated; PTH INCREASES the calcium reabsorption here
- note that 92% of calcium is coupled with Na+; the 8% in the distal tubule is NOT - this is why thiazide diuretics are Ca2+ sparing
66
Where is magnesium mostly reabsorbed?
- in the ascending limb of the loop of Henle!
- 60% is reabsorbed here, 30% in the proximal tubule, and 5% in the distal tubule (95% total)
- this means that loop diuretics strongly inhibit Mg2+ reabsorption
- (note that Mg2+ reabsorption in the loop of Henle is paracellular)
