ICL 1.3: Renal Physiology II

Question 1

what is tubular reabsorption?

Answer 1

almost all the H2O and the majority of salt/solutes are reabsorbed and most of this reabsorption is in the proximal tubule!!

reabsorption of: glucose, AA, proteins, vitamins, lactate, urea, uric acid, Na+, K+, Ca+2, Mg+2, Cl-, HCO3-, H2O

reabsorption in the PCT is iso-osmotic!!! so there’s no change in the osmolarity of the PCT glomerular filtrate vs the blood –> but beyond the PCT, reabsorption is NOT iso-osmotic because there’s stuff being reabsorbed without it being balanced out and it’s not the same osmolality as the plasma

some secretion happens in the PCT but not much, just urea, uric acid, creatinine and some drugs

Question 2

which molecules are freely filtered?

Answer 2

1. electrolytes: Na, K, Cl, HCO3
2. metabolic waste: urea, creatinine
3. metabolites: Glucose, AA, organic acids
4. small proteins and peptides: Insulin, myoglobin

Question 3

which molecules are not freely filtered?

Answer 3

1. plasma proteins: albumin

2. lipid soluble substances attached to proteins: thyroxine, hormones, bilirubin

Question 4

a substance is freely filtered. which of the following would have the same concentration for this substance as the peripheral plasma?

A. glomerular filtrate

B. afferent arteriole

C. efferent arteriole

D. all of the above

Answer 4

D. all of the above

the concentration of ANY substance that is freely filtered is the same proportion as water in the blood!

PCT is not in the same proportion as water; glucose is absorbed more than water in the PCT – but osmolarity will be the same

Question 5

what are the properties of the cortex?

Answer 5

1. vascular endothelium (peritubular capillaries) is fenestrated and allows for reabsorption –> this isn’t a thing in the medulla
2. transport is governed almost exclusively by events in the tubular epithelium
3. cortical interstitium has an osmolality and small solute concentration close to plasma!

Question 6

what are the properties of the medulla?

Answer 6

1. only some regions of the vasculature fenestrated
2. blood flow and transport events are less rapid
3. transport depend on BOTH the vascular endothelium and tubular epithelium
4. medullary interstitium NOTplasma-like in composition; it has high salt concentration and high osmolarity!

Question 7

what are the dominant mechanisms of tubular reabsorption?

Answer 7

1. paracellulartransport across the epithelium by passing through the intercellular space between the cells.
2. transcellular transport: movement THROUGH cells via passive diffusion or active transport

they have to cross two membranes: through apical membrane into the cell & then through basolateral membrane

both methods are highly regulated!!

Question 8

the functioning of what is critical for the paracellular movement of water across the nephron tubule?

Answer 8

Na+/K+ ATPase pump

it actively pumps Na+ out into the blood and reabsorbs it so water follows the gradient and is also reabsorbed!

Question 9

how is tubular reabsorption regulated?

Answer 9

it’s regulated by multiple nervous, hormonal, and local control mechanisms

the nice thing is that reabsorption of some solutes can be regulated independently of others –> if there’s a lot of Na+ in your body and you want to excrete it but you don’t want to lose Cl- or K+ then you can excrete the Na+ without losing the other ions too

glomerulotubular balance = ability of the tubules (mainly proximal ) to increase the reabsorption rate with increased tubular load (% of GFR reabsorbed remains constant) –> so if your GFR changes and it isn’t accompanied by an increase in tubular reabsorption you’ll be losing a lot of important stuff!

it buffers the effects of spontaneous changes in GFR on urine output like autoregulatory mechanisms (tubuloglomerular feedback)

Question 10

what might be regulated by the tubuloglomerular feedback?

A. GFR

B. tubular reabsorption

Answer 10

A. GFR

signal is coming from the tubule to the glomerulus so filtration happens at the glomerulus

Question 11

what might be regulated by the glomerulotubular feedback?

A. GFR

B. tubular reabsorption

Answer 11

B. tubular reabsorption

singnal is coming from the glomerulus to the tubule and reabsorption is what happens in the tubule

Question 12

what’s the difference in the Starling forces of the glomerulus vs. the peritubular capillaries?

Answer 12

Bowman’s space oncotic pressure was missing in the glomerulus because there was no protein filtration but in the capillaries, the interstitium DOES have oncotic pressure!

reabsorption = Kf x net reabsorptive force

so increased capillary oncotic pressure and increase insterstial hydrostatic pressure would favor net reabsorption!

Question 13

what is the equation for the net reabsorption pressure?

Answer 13

NRP = Pif + πc - Pc - πif

Pif = hydrostatic pressure in the renal interstitium

πc = colloid osmotic pressure of the peritubular capillary

Pc = peritubular hydrostatic pressure

πif = colloid osmotic pressure in the renal interstitum

renal tubule | renal interstitium | peritubular capillary

Question 14

peritibular capillary reabsorption is directly influenced by changes in what?

Answer 14

peritibular capillary reabsorption is directly influenced by changes in:

1. peritubular capillary hydrostatic pressure

if you decreased glomerular hydrostatic pressure by constricting afferent arteriole, that pressure in the glomerulus is what’s carried over to the peritubular capillaries through the efferent arteriole

if the afferent arteriole is dilated then glomerular hydrostatic pressure is going to be increased and so will the hydrostatic pressure in the particular capillaries!

2. peritubular capillary colloid oncotic pressure

FF increases the concentration of protein and increases oncotic pressure so anything that increase FF will increase colloid osmotic pressure in the peritubular capillaries which favors reabsorption! high FF = more reabsorption

Question 15

what determines the peritubular capillary hydrostatic pressure?

Answer 15

arterial pressure and afferent and efferent arteriolar resistance!

increased arterial pressure –> increased peritubular capillary hydrostatic pressure –> decreased reabsorption rate

increased arteriolar resistance in afferent and efferent –> decreased peritubular capillary hydrostatic pressure –> increased reabsorption rate

so in the PCT you want to reabsorb into the capillaries but in the glomerulus you want high hydrostatic pressure to favor filtration into the Bowman’s space

Question 16

what determines the peritubular capillary colloid pressure?

Answer 16

peritubular capillary colloid pressure is determined by systemic plasma colloid osmotic pressure and filtration fraction

increase in systemic plasma protein concentration –> increased peritubular capillary colloid osmotic pressure –> increased reabsorption

increased FF –> increased peritubular capillary colloid osmotic pressure –> increased reabsorption

FF = GFR/RPF

angiotensin II increases peritubular capillary reabsorption by decreasing RPF

Question 17

how does the peritubular capillary filtration coefficient effect reabsorption in the PCT?

Answer 17

Kf is a measure of the permeability and surface area of the capillaries

increased Kf = increased reabsorption

decreased Kf = decreased reabsorption

Kf remains relatively constant in most physiological conditions though

Question 18

which of the following factors would increase reabsorption at the peritubular capillaries?

A. constriction of efferent arterioles

B. dilation of efferent arterioles

C. constriction of afferent arterioles

D. dilation of afferent arterioles

Answer 18

A and C

constriction of the efferent AND afferent arterioles; both would decrease hydrostatic pressure in the peritubular capillaries which increases reabsorption!

angiotensin preferentially constricts the efferent arterioles and increases reabsorption but it also increases FF which increases colloid oncotic pressure! so it decreases hydrostatic pressure and increases oncotic pressure for overall increased reabsorption

Question 19

how much is taken up by the peritubular capillaries?

Answer 19

uptake by the peritubular capillaries closely matches the net reabsorption from the tubular lumen into the interstitium

it’s determined by changes in the hydrostatic and colloid osmotic pressures

1. forces that increase peritubular capillary reabsorption also increase reabsorption from the renal tubules
2. changes that inhibit peritubular capillary reabsorption also inhibit tubular reabsorption

Question 20

what is back leak?

Answer 20

as solutes enter renal interstitium from the lumen, H2O follows by osmosis

from the interstitium, they can move to the peritubular capillaries or back into the tubular lumen since “tight” junctions are leaky and allow diffusion in both directions

with the normal high rate of peritubular capillaryreabsorption, the net movement is into the peritubular capillaries with little backleak because reabsorption is favored

however, when peritubular capillaryreabsorption is reduced, backleak increases leading to reduced rate of netreabsorption

Question 21

what is pressure natriuresis and pressure diuresis?

Answer 21

natriuresis = loss of Na+ and diuresis = loss of water

if you have an increase in arterial pressure, it increases glomerular hydrostatic pressure and increased GFR but it also increases the peritubular hydrostatic pressure which means less reabsorption! so molecules will get filtered more and not reabsorbed (usually this doesn’t happen because of autoregulation via RAAS and adenosine/ATP pathways)

but in this condition, small increases in arterial pressure can cause large increase in urinary excretion of Na+ and water

when autoregulation is impaired, slight increase in peritubular capillary hydrostatic pressure and a subsequent increase in the renal interstitial fluid hydrostatic pressure leads to large increases in GFR and decreased Na+ and H2O reabsorption. This increases backleak of sodium into the tubular lumen and reduces the netreabsorption of sodium and water

anything that causes reduced angiotensin II formation leads to decreased tubular sodiumreabsorption(and water)

Question 22

how do transporters limit the rate of reabsorption?

Answer 22

the rate of reabsorption limited by the capacity of the transporters! tight junctions are impermeable to the solutes so the limit on their transport rate is set by the capacity of the transporters

if there aren’t enough transporters then excess of whatever there is will be lost in the urine; so if the filtered load > Tm, solutes are excreted

reabsorption increases until transports are saturated!

if the filtered load < Tm then these solutes will be complete reabsorbed!

ex. glucose

Question 23

when plasma glucose reaches such high levels that substantial amount of glucose appears in the urine, what happens?

A. glucose is leaked back into the tubule through tight junctions

B. there is not enough luminal sodium to move in symport with glucose

C. all the glucose transporters are working at their maximum rate

D. the glucose transports are being inhibited by the high levels of glucose

Answer 23

C. all the goose transporters are working at their maximum rate

glucose can’t leak because it’s too large for the tight junctions so there’s no backleak

Question 24

how does the gradient limit the rate of transport?

Answer 24

the rate of reabsorption limited by paracellular back leak (gradient-limited)

tight junctions re leaky and as the substance is reabsorbed the gradient between the two media (luminal and interstitial) increases which causes backleak so that the luminal and interstitial concentrations remain close

since water is being reabsorbed, reabsorption does not stop! the limiting gradient will be reached if water reabsorption is stopped

these solutes are NEVER reabsorbed completely!!

ex. sodium

Question 25

major reabsorption occurs in what part of the nephron?

Answer 25

major reabsorption occurs in the proximal tubules!! it’s the major site for reabsorption of organic nutrients

65% of the filtered load of Na+ and H2O are reabsorbed by the proximal tubule

the PCT cells are highly metabolic and have large numbers of mitochondria to support powerful active transport processes

the cells have an extensive brush border on the luminal (apical) side of the membrane and intercellular and basal channels

epithelial brush border loaded with protein carriers

Question 26

which solutes get reabsorbed in the proximal tubule?

Answer 26

1. Na+
2. Cl-
3. HCO3-
4. K+
5. H2O
6. glucose
7. AA

H+, organic acids and bases get excreted back into the lumen

Question 27

In what proportion is Na+ reabsorbed in the PCT?

Answer 27

Na+ is absorbed in proportion to H2O

this means that the osmolarity remains constant in the PCT because the same amount of Na+ and H2O are getting reabsorbed together

Question 28

in what proportion are organic solutes like glucose, AA, and HCO3- reabsorbed in the PCT? how does this effect their concentration along the PCT?

Answer 28

glucose, AA, HCO3- are reabsorbed more than H2O!!

so their concentration decreases along the PCT because they’re getting reabsorbed into the peritubular capillaries

organic solutes that are not actively reabsorbed like urea and creatinine increase their concentration along the PCT

Question 29

which of the following moelcules is absorbed more in proportion to water in the PCT?

A. glucose

B. Na+

C. K+

D. Cl-

Answer 29

A. glucose

so its concentration decreases along the PCT

Na+, K+ and Cl- are reabsorbed int the same proportion as water in the PCT!!

Question 30

which of the following molecules is absorbed less in proportion to water in the PCT?

A. Na+

B. urea

C. amino acids

D. Cl

Answer 30

B. urea

so its concentration increases along the PCT

Question 31

T/F: HCO3- is absorbed in the same proportion to water in the PCT

Answer 31

False

it’s absorbed more so its concentration decreases along the PCT

Question 32

how i glucose handled by the kidney?

Answer 32

the kidneys normally reabsorbs all the glucose that is filtered –> it is taken up across the apical membrane by sodium-glucose symporters (SGLT) and leaves across the basolateral membrane via glucose uniporters (GLUT family)

in most of the proximal tubule the sodium-glucose stoichiometry is one-for-one (SGLT-2 isoform) –> SGLT2 is closer to the glomerulus and it doesn’t have as much affinity as SGLT1 so it’s more efficient because for every Na+ a glucose can be reabsorbed too but since it isn’t as high of an affinity, some glucose molecules may escape reabsorption

in the late proximal tubule the stoichiometry is two-for-one (SGLT-1 isoform) and it has super high affinity for glucose and will bind glucose no matter how low the concentration but it isn’t as efficient and needs 2 Na+ to get it reabsorbed

Question 33

what is glycosuria?

Answer 33

at a given GFR, rate of glucose filtration ∞ plasma glucose concentration

at normal plasma glucose levels, all the filtered glucose is reabsorbed and none excreted

when rate of glucose filtration > Tm; excess glucose filtered is excreted (glycosuria)

abnormally high filtered loads (plasma glucose > 200 mg/dL) in untreated diabetes mellitus –> in very severe cases plasma glucose > 1000 mg/dL

there is no backleak of glucose since the tight junctions are impermeable to glucose

Question 34

what are SGLT-2 inhibitors?

Answer 34

SGLT-2 inhibitors (glyflozins) lead to excretion of a large fraction of the filtered load of glucose.

useful for treating type 2 diabetes!

Question 35

how does the kidney handle proteins and peptides?

Answer 35

peptides and smaller proteins (angiotensin,insulin etc) and a small amount of large plasma proteins (eg: 0.02% albumin) gets filtered

larger proteins undergo endocytosis (specific receptors on the apical membrane); the rate of endocytosis limited by Tm

very small peptides are catabolized into amino acids or di- and tripeptides within the proximal tubular lumen by peptidases located on the apical surface –> reabsorption of amino acids by specific transporters on the apical surface

Question 36

what is proteinuria?

Answer 36

urinary protein excretion of > 150mg/day

powerful predictor of progressive renal disease

hallmark of diabetic and hypertensive nephropathy

Question 37

what is Fanconi syndrome?

Answer 37

defect in PCT reabsorption which leads to excretion of glucose, HCO3, AA, and phosphate so they’ll appear in the urine

may lead to proximal renal tubular acidosis (type II RTA)

can be caused by exposure to certain drugs/heavy metals, vitamin D deficiency, kidney transplant, MM, amyloidosis

Question 38

does secretion happen in the PCT?

Answer 38

PCT is important for secretion of many metabolism end products (bile salts,oxalate,urate, catecholamines etc.)

kidneys also secrete many potentially harmful drugs or toxins directly through the tubular cells into the tubules

rapid clearance of certain drugs, such as penicillin and salicylates by the kidneys creates a challenge in maintaining a therapeutically effective drug concentration

Question 39

how are organic cations vs anions secreted?

Answer 39

secretion of organic cations is energetically favorable because of the Na/K ATPase pump which pumps 3Na+ out with 2K+ in which makes the inside of renal interstitum negative so the + ions can come in from the capillaries to the interstitium and then the hydrogen/cation exchanger dumps the cations into the lumen of the PCT

anion secretion isn’t as easy because it’s not energetically favorable due to the negative charge in the cell – so there’s an active alpha-KG pump that cotransports 3Na+ and 1 (-) alpha-KG molecule into the cell –> now you’ve made a gradient and alpha-KG will move out of the cell back into the capillaries down its gradient and a (-) cation will replace it in the lumen via an OAT transporter

Question 40

how are organic cations secreted?

Answer 40

there are several nonselective transport systems for organic cations in the PCT; Tm very high and > 90% removed

the process begins with the Na-K-ATPase establishing a negative membrane potential

organic cations enter across the basolateral membrane via uniporters, members of the OCT family (OrganicCationTransporter) and then they exit into the lumen via an antiporter that exchanges a proton for the organic cation

maintains electrical neutrality

Question 41

which drugs and endogenous substances are organic cations?

Answer 41

DRUGS

1. atropine
2. isoproterenol
3. cimetidine
4. moprhine

ENDOGENOUS

1. ACh
2. choline
3. creatinine
4. dopamine
5. epinephrine
6. histamine
7. serotonin
8. thiamine

Question 42

how are organic anions secreted?

Answer 42

the active secretory pathway for organic anions in the PCT uses the recycling of α-ketoglutarate (αKG)

first, αKG, is actively taken up from both the lumen and interstitium by a Na+/αGK symporter which raises its cellular levels.

then αKG then crosses the basolateral membrane via an antiporter; OrganicAnionTransporter (OAT) that ALSO imports an organic anion

the organic solute is secreted across the apical membrane via one of several pathways

the basolateral membrane of proximal convoluted tubule epithelial cells contains several OAT isoforms and the PCT can secrete all the organic anions

transport is limited by aTm

if the plasma concentration of an organic anion is too high, it will not be efficiently removed

Question 43

which drugs and endogenous substances are organic anions?

Answer 43

DRUGS

1. acetazolamide
2. cholorothiazide
3. furosemide
4. penicillin
5. saccharin

ENDOGENOUS

1. bile salts
2. fatty acids
3. oxalate
4. prostaglandins
5. urate

Question 44

why is potassium regulation so important?

Answer 44

K + is a major component of the intracellular fluid (ICF); ~ 2% in extracellular fluid (ECF)

IF [K+] : ECF [K+] is the major determinant of the resting membrane potential in nerve and muscle cells

maintenance of K+ balance depends primarily on kidneys (feces only excretes ~ 5 - 10 % ofK+)

failure to adjust K+ balance could be life-threatening

hyperkalemia/ hypokalemia need medical intervention

redistribution of K+ between the ICF and ECF is the first line of defense against [K+] changes

most of the ingested ECF rapidly moves into the cells until the kidneys can eliminate the excess K+

Question 45

how does the kidney handle K+?

Answer 45

glomerular filtration –> early proximal reabsorption followed by secretion –> reabsorption in the thick ascending Loop

distal secretion predominantly by principal cells of the cortical collecting duct

Question 46

what are the two types of special channels allow K+ diffusion into the PCT?

Answer 46

two types of special channels allow K+ diffusion into the PCT:
1. renal outer medullary K+ (ROMK)

2. high conductance“big” K+ (BK) or Maxi-K+ channels

so these two channels allow for lots of K+ secretion in the PCT

Question 47

how is K+ reabsorbed in the PCT?

Answer 47

K+reabsorption in PCT mostly paracellularly

active Na+reabsorption drives H2O and takes K+through solvent drag

there is some transcellular K+transport

K+inside from the Na+/K+- ATPase pump exit the basolateral membrane through a conductive pathway or coupled to Cl-

Question 48

how is K+ reabsorbed in the thick ascending loop?

Answer 48

K+reabsorption through paracellular and transcellular mechanisms

transcellular mechanism is accomplished via apical Na+/K+/2Cl−cotransporter

ROMK channel recycles K+back into the lumen and sustains Na+/K+/2Cl−cotransport

K+also exits the cell through cotransport with Cl−.

Question 49

how is K+ secreted in the early distal tubule?

Answer 49

K+/Cl−cotransport is present on apical surface of the DCT and collecting duct and transports K and Cl into the lumen

ROMK is expressed throughout the DCT and into the cortical collecting duct on the apical surface as well and transport K into the lumen

conditions that cause a low luminal Cl−concentration increase K+secretion –> this is because there is a Na/Cl cotransporter than is taking Na and Cl rom the lumen to the blood and a Cl-/K cotransporter taking Cl and K from the interstitum to the lumen so if there’s low Cl- in the lumen this means the Cl/K pump will work more and excrete more Cl- and K+ so that there’s enough Cl- in the lumen for the Na/Cl cotransport to work

high HCO3- = low Cl- so alkalosis leads to hypokalemia!!

Question 50

how is K+ secreted in the late distal tubule?

Answer 50

there’s an ENaC transporter of Na+ from the lumen to the interstitum

there’s a ROMK transporter that pumps K+ from the interstitium to the lumen

there’s a Cl/K cotransporter that pumps K and Cl from the interstitium to the lumen

so if you have hyperkalemia you’ll actively secrete K but that means you’re losing Cl- too which means gain of bicarbonate!! so you’ll become alkalemic

Question 51

what are the 2 main cells types of the late distal and cortical collecting tubules? what do they do

Answer 51

1. intercalated cells reabsorb or secrete K+

in severe K+ depletion, K+ secretion stops and there is a net reabsorption through thetype A intercalated cells

with excess K+ in the body fluids,type B intercalated cellsactively secrete K+ into the lumen (functions opposite to type A cells)

2. principal cells secrete K+

under the control of
- activity of Na/K-ATPase pump

• electrochemical gradient
• permeability of the luminal membrane

Question 52

how is K+ secreted in the collecting duct?

Answer 52

K+secretion in the initial collecting duct and the cortical collecting duct is through the principal cell

basolateral Na+/K+-ATPase creates a favorable diffusion gradient for movement of K+from the cell into the lumen through well defined channels

ROMK and Maxi-K transport K+ into the lumen, ENac transports Na+ into the interstitum, Cl/K cotransports them into the lumen

Question 53

how is K+ transported in the collecting duct?

Answer 53

in the intercalated cells, H+/K+-ATPase secrete H+ and reabsorb K+in an electroneutral fashion

the activity of the H+/K+-ATPase increases in K+depletion

K+depletion enhances collecting duct H+secretion so when you’re low on potassium, you’ll secrete H+ and cause alkalosis

reabsorption of HCO3in the distal nephron is mediated by apical H+secretion by theα-intercalated cell

Question 54

what are ROMK and Maxi-K channels?

Answer 54

ROMK and Maxi-K transport K+ into the lumen so when the body is trying to conserve K+ ROMK channels are mostly sequestered in intracellular vesicles and BK channels are closed so there’s no secretion of K+!

under normal conditions, ROMK channels secrete K+ but BK channels remain closed

with a high K+ diet, ROMK channel activity is maximized and BK channels are open so there’s substantial K+ secretion

Question 55

what is happening that would cause potassium excretion to be low? aka where and how is it being rebabsorbed in all the different parts of the nephron?

Answer 55

1. when potassium excretion is low, the majority of filtered potassium is reabsorbed in the proximal tubule, mainly by the paracellular route
2. in the thick ascending limb most of the rest is reabsorbed, mostly by the transcellular route via Na/K/2Cl transporter
3. in the cortical and medullary collecting duct there is some additional reabsorption via intercalated cells via the H/K ATPase pump

Question 56

what happens when potassium excretion is high?

Answer 56

when potassium excretion is high, same events in most regions of the tubule but in the distal nephron there is major secretion (5) that in some cases is greater than the sum of the reabsorptive processes

Question 57

how is K+ filtered at different locations depending on diet?

Answer 57

NORMAL/HIGH K+
1. PCT = 65% reabsorption

2. thick ascending limb = 25% reabsorption
3. distal tubule and principal cells in the connective tubule and cortical collecting duct = 20-150% secretion
4. intercalated cells, medullary collecting duct = 5% reabsorption
5. final urine = 20-150%

LOW K+
1. PCT = 65% reabsorption

2. thick ascending limb = 25% reabsorption
3. distal tubule and principal cells in the connective tubule and cortical collecting duct = low secretion
4. intercalated cells, cortical collecting duct = 5% reabsorption
5. intercalated cells, medullary collecting duct = 3% reabsorption
6. final urine = 2%

Question 58

how is potassium homeostasis associated with acid-base balance?

Answer 58

in general:

1. acidemia (reduced blood pH) is associated with increased plasma [K]- hyperkalemia
2. alkalemia (increased blood pH) is associated with reduced plasma [K]- hypokalemia

this is because of the H/K ATPase pump in the collecting duct; when H+ is high and you have acidosis, this pump will activate and H+ will get pumped out but in exchange K+ will be pumped in an you’ll get hyperkalemia

metabolic acidosis can cause hyperkalemia

high plasma [K+] can induce a mild metabolic acidosis

metabolic alkalosis causes K+ movement into the cells

hypokalemia causes H+ movement into the cells

Question 59

how does the kidney regulate potassium in the distal nephron? aka what factors increase vs. decrease K+ secretion?

Answer 59

low plasma K and angiotensin II will decrease K secretion

high Na+ delivery to principal cells, aldosterone, high plasma K+ and GI hormones increase K+ secretion in the distal nephron

Question 60

how does angiotensin effect K+ secretion?

Answer 60

antgiotensin II decreases K+ secretion

it decreases the activity of ROMK channels in principal cells

Question 61

how does aldosterone effect K+ secretion?

Answer 61

aldosterone stimulates K+ secretion

1. stimulates active reabsorption of Na through Na/K ATPase pump
2. increase the number of K+ channels in the luminal membrane and thus its permeability

Question 62

how does Na+ delivery to the distal nephron effect K+ secretion?

Answer 62

high Na+ delivery stimulates K+ secretion; low Na+ delivery inhibits it –> the influence is exerted on both principal and intercalated cells

in principal cells, Na entry increases the electrochemical gradient driving the outward flow of K through ROMK channels –> more Na+ delivered means more Na+ taken up and pumped out by the Na-K-ATPase, causing more K+ to be pumped in

in type A intercalated cells, in conditions of high Na+ delivery, the BK channels become activated and secrete potassium in addition to the ROMK channels in principal cells

Question 63

how does distal tubular flow rate effect K+ secretion?

Answer 63

increased distal tubular flow rate stimulates K_ secretion

decrease in distal tubular flow rate reduces K+ secretion and it’s strongly influenced by K+ intake

with high potassium, increased tubular flow rate has more effect than with low K+ intake –> increased number of high conductance BK channels in the luminal membrane.

Question 64

how do loop diuretics and thiazide diuretics effect K+ levels?

Answer 64

loop diuretics cause K+ depletion because they block K+ reabsorption in the thick ascending limb

for both classes of diuretics the major factor leading to increased K+ excretion is:

1. increased delivery of sodium to principal cells
2. increased luminal flow in the distal nephron

Question 65

where does maximum Mg+2 reabsorption occur in a nephron?

Answer 65

thick ascending limb of the loop of henle

most other ions it’s PCT but Mg+2 is the TAL

Question 66

what happens to the bound Ca+2 levels in alkalosis?

Answer 66

increases

it decreases in acidosis

Question 67

how does PTH effect phosphate absorption in the kidney?

Answer 67

PTH decreases reabsorption

Question 68

how does PTH effect blood phosphate level?

Answer 68

PTH does not change the blood phosphate level much

even though it increases phosphate secretion, it also causes increased phosphate release from bone

Question 69

how does calcitonin effect calcium and phosphate reabsorption?

Answer 69

calcitonin decreases the reabsorption of calcium and phosphate

because calci”tonin” tones them down

Question 70

what decreases Ca+2 reabsorption but increases phosphate excretion by the kidney?

Answer 70

calcitonin

calcitonin doesn’t increase absorption, it decreases reabsorption which means increased excretion

calcitonin decreases the reabsorption of calcium and phosphate; calcitonin does NOT increase secretion

Question 71

handling of calcium in which segment of the nephron is affected by the hormone PTH?

Answer 71

distal tubule

PTH increases calcium reabsorption in the distal tubule

Question 72

which ion is essential for calcium, phosphate and magnesium reabsorption in the PCT?

Answer 72

Na+

phosphate is reabsorbed via Na/PO4 transporter

Mg follows when Na is absorbed and takes H2O with it

Ca mechanism is not known but when there’s less Na+ there’s also less Ca+2 reabsorption

Question 73

what increases calcium excretion?

Answer 73

1. acidosis
2. fluid expansion
3. hypercalcemia
4. loop diuretics

loop diuretics inhibit Na/K/Cl transport so the lumen’s negative charge is lost and Ca+2 reabsorption is effected

Question 74

do thiazide diuretics cause hyper or hypocalcemia?

Answer 74

hypercalcemia

they competitively inhibit Na/Cl transporter and so the Na isn’t reabsorbed and when that happens, Ca+2 is reabsorbed more instead and it causes hypercalcemia

Question 75

why is correcting Mg+2 first important in correcting hypocalcemia if both are low in blood?

Answer 75

Mg+2 helps induce PTH secretion

PTH releases Ca+2 by increases reabsorption and increases release of Ca+2 from the bones!

so normalizing the Mg+2 normalizes the Ca+2

Question 76

which enzyme is necessary for the formation of vitamin D in the kidney?

Answer 76

1-alpha-hydroxylase

Question 77

for which substance is it possible to excrete more than is filtered?

A. K+

B. Mg+2

C. Ca+2

D. phosphate

Answer 77

K+

you can secrete up to 150%