Physio - Kidney

Front 1

What is role of renin-angiotensin-aldosterone system (RAAS)?

Back 1

RAAS plays important role in regulating blood volume and SVR, which together influence CO and arterial pressure.

Essentially, their primary function is to incr. H2O and NaCl reabsorption.

Front 2

macula densa
where located?

Back 2

area of closely packed specialized cells lining DISTAL TUBULE (ascending loop) where loops back adjacent to vascular pole (afferent and efferent arteriole) of parent glomerulus,

Front 3

Cells of macula densa are packed in distal tubule where runs near glomerus & JG cells between AA and EA.
Regarding the function of the macula densa cells...
►What tubular fluid change (stimuli) do these cells respond to?
►Macula densa cells and JG apparatus respond to these changes through what 2 mechanisms?

Back 3

* Macula Densa cells respond to Na & Cl ion levels in tubular fluid (osmoreceptors).
* If reduction in tubular NaCl detected by MD cells -> produce molecular signals --> stimulating (1)renin release from nearby JG cells into circulation

Also (2)afferent arteriole will dialate as part of intrinsic regulation of GFR. (effects explained in later question)

Front 4

So renin is released by macula densa cells??

Back 4

No!...renin release from nearby JG cells into circulation

Front 5

Peritubular capillary pressure (capillaries around renal tubules) is higher OR lower than other capillaries in body?

Back 5

LOWER blood pressure than other capillaries in the body; supports reabsorption!!!

Front 6

Is Na+ conc. higher in tubular cell (epithelium lining tubules) OR is it higher in interstitium?

Why significant?

Back 6

Sodium conc. higher in interstitium. Therefore, Na+ must be actively transported (Na/K pump) in order to move ions from tubular cells into interstitial fluid, etc.

However, it passively moves from tubular lumen into epithelium, and from interstitium into peritubular capillary.

Front 7

How are MD cells involved in autoregulation of GFR?

Back 7

Tubulooglomerular feedback mechanism:

When GFR high, insufficient time for peritubular capillaries to reabsorb, and concentration of solutes in tubules stays high.
MD stimulated and somehow vasocontrictors (of afferent arteriole) released .

Front 8

Again...JG cells contain what? Where located?

Back 8

•JG cells (granular) contain RENIN
•Located in smooth muscle near arteriole walls

Front 9

HA (weak acid) <-- ---> (H+) + (HCO3-)

Weak acid is only partially dissociated in solution..
What happens when more H+ is added to solution?

Back 9

Reaction shift to left

More undissociated HA

Front 10

HA (weak acid) <-- ---> (H+) + (HCO3-)

Weak acid is only partially dissociated in solution..
What happens when H+ is taken from solution (e.g. by kidney)?

Back 10

RxN shifts to right

More demand for dissociated H+, cause more bases and/or anions will be present

Front 11

What are 2 of most important intracellular buffers?

Back 11

proteins e.g. hemoglobin
also phosphate (as urinary buffer)

Front 12

What is only open buffer system in body?

Back 12

bicarb system, b/c both components are regulated
(expand on this further)

CO2 by lungs
HCO3- by kidney

Front 13

Respiratory acidosis occurs when..?

Back 13

lungs NOT removing CO2 quickly enough

for example after hypoventilation

Front 14

Respiratory alkalosis occurs when..?

Back 14

lungs removing CO2 faster than it can be produced

e.g. in hyperventilation

Front 15

Drop in plasma K+ (hypokalemia) causes...

Back 15

K+ must leave cells, coupled with H+ influx. Change in intracellular H+ leads to secretion of H+ into tubule/urine, b/c some + has to leave to make room for K+...Thus metabolic alkalosis arises due removal of H+ ions.

Conversely, hyperkalemia leads to metabolic acidosis

Front 16

Increased aldersterone concentrations do what to K+ secretions?

What is end result?

Back 16

increase them, filtration incr and peritubular capillaries can only reabsorb so fast :(

this leads to hypokalemia (metabolic alkalosis - which is also b/c Na+ reabs and H+ leaves p.445)

Front 17

Glom.filtration is ______ process in which H2O and nearly all subst. in plasma move together (not really selective permeable).

Back 17

bulk flow process p.372

reabsorption on other hand is a selective process

Front 18

How do u calculate [renal] plasma flow from [renal] blood flow?

Back 18

Need to know hematocrit.
Multiply 1-HCT% by volume of blood.

e.g. 1000ml/min * 0.6 = 600ml/min

Front 19

Which structure(s) appears first on tubular system: peritubular capillaries OR juxtamedullary apparatus?

Back 19

peritubular capillaries; wraps around PCT

JGA (site of JG and MD cells) is where distal tubule runs between efferent and afferent arteriole.

Front 20

What is descending LoH impermeable to?

Back 20

Na+
(but 2/3 leaves before LoH in PCT)

Front 21

What is ascending LoH impermeable to?

Back 21

H2O

Front 22

What is osmolarity of tubule entering LoH?

What is osmolarity of tubule leaving LoH before DCT?

Back 22

300

100
Then it goes way up in collecting duct as H2O leaves, amount depending on how much ADH acting on it...

Front 23

Approx. how much blood is filtered by kidney (dog) per minute?

Back 23

80L/24 hrs OR 50mL/min (i believe)

Front 24

Where part of tubule does alderstone act on?
What does it incr? Decreases?

Back 24

• Aldersterone is most important determinant of renal Na+ reabsorption
...Aldosterone is a SODIUM SAVER...remember A-S-S

• acts on DISTAL tubule and collecting duct

• Increases NaCl and H2O reabsorption....decreases K+ reabsorption

Front 25

Where on tubule is AT2 act?

What does it incr? decr?

Back 25

AT2 stimulates secretion of aldersterone

PT, thick ascending, LoH, DT

increases NaCl and H2O resorption in 2 ways

1. (indirectly by stimulating release of aldrerstone)
2. constricting afferent / efferent arterioles, reducing pressure in peritubular caps., promoting reabs.
(for whatever reason, book says doesn't have much affect on GFR)
Decreases hydrogen (b/c its puumped back in)

Easy. You reabsorb Na+, then water and other solutes follow.

Front 26

What part of renal tubule does ADH act on?

What does it incr? decr?

Back 26

acts on distal tubule and collecting duct

increases H2O reabsorption

Front 27

ANF is what? Opposes what?

Decreases what?

Back 27

diuretic which opposes aldersterone

decreases salt, H2O absorption

Front 28

PTH acts on what part of tubular system?
stimulates abs. of?
decreases reabs. of?

Back 28

PT, thick ascending, LoH, DT

increases calcium abs.

decreases phosphate reabs, b/c binds with H+ and gets excreted

Front 29

Which cells contain renin?

What kind of cells are they? Describe them.

Back 29

Juxtaglomerular cells (or granular cells) are smooth muscle cells on afferent arteriole...JG cells stimulated by MD cells.

Front 30

What stimulates release of renin? (name three factors)

Back 30

decr in blood vol

In more detail:
Peptide hormone is secreted by kidney from specialized cells called granular cells of JGA via 3 responses:

* 1) A decrease in arterial BP (that could be related to a decrease in blood volume) as detected by baroreceptors (pressure-sensitive cells). This is most causal link between BP and renin secretion (other two methods operate via longer pathways).
* 2) A decrease in NaCl levels in ultra-filtrate of nephron. This flow is measured by macula densa of JGA.
* 3) Sympathetic nervous system activity, which also controls BP, acting through beta1 adrenergic receptors.

Front 31

1. Define renal clearance:

2. if "creatine clearance is 120", what does this mean?

Back 31

1. Volume of plasma cleared of substance (e.g. creatine) per minute

2. clearance of 120 = 120mL of plasma cleared of creatine per minute

Front 32

What substance gets excreted at 100% of volume entering filterate and secreted actively from peritubules (100% remaining renal plasma flow) until carriers are saturated?

Back 32

PAH

fyi: can be used to calculate renal plasma flow b/c all PAH that flows through glomerulus (remainder secreted) is excreted; clearance of PAH (Cpah) = RPM

Front 33

What is formulas for renal clearance?

Back 33

Clearance = urine conc. (mg/mL) x urine flow (mL/min) / plasma conc. (mg/mL)

Front 34

Why is creatine great indication of GFR?

Back 34

Produced by body and filtered 100%, but not secreted or reabsorbed.

Front 35

Sample question:
PAH plasma conc. 0.2mg/ml
PAH urine conc. 120mg/ml
urine flow of 1mL/min
HCt = 0.4
> determine renal BLOOD flow:

Back 35

Clearence = 600ml/min <plasma flow
(600ml/min) / 0.6= 1000ml/min renal blood flow

Front 36

clearance ratio
if clearance is greater than 1

if clearaance is less than 1

Back 36

filtered and secreted

filtered and absorbed

Front 37

Approximately what percentage of plasma passing through DOG kidney is filtered thr. glomerulus?

Back 37

25%, generate 55ml of filtrate per minute from 220ml of plasma (400ml of blood).

Remaining 165 ml (75%) goes to peritubular capillaries.

(horse filters only 10%)

Front 38

3 layers of glomerular "filter"?

Back 38

1. endothelium
2. podocytes
3. basal lamina (basement membrane)

Front 39

3 physiological mechanisms or conditions affecting GFR

Back 39

1. autoregulation
2. angiotension 2 -
3. sympathetic nerve fibers

Front 40

Where are Na/K pumps located on renal tubules?
(And more specifically where in cell membrane?)

Back 40

Unlike most cells in body, Na/K pump not evenly distributed in cell membrane of renal tubular cells. Only present on basolateral membrane (NOT apical/luminal side).

Found on PT (primary location near peritubular capillaries), ascending limb of LoH, and of course DT.

Front 41

Challenge Question:
An increase in plasma K+ has what affect on aldersterone?

What negative effects does hyperkalemia (high K+ in blood) have on heart?

Back 41

Aldersterone is SODIUM SAVER and stimulates K+ secretion;

K+ conc. should be higher in cells, not interstitium or plasma. If too high in plasma, can cause heart arrhythmias and weak heart contractions.

See page 451 in text.

Front 42

3 hormones that act of DT and collecting duct

Back 42

ADH, ANF, aldersterone

fyi: in pic adh = avp

Front 43

Describe mov't of urea during "recycling" routine?

Significance or purpose of this?

Back 43

DT and proximal (top) of CD impermeable to urea, so only H2O leaves. Osmolarity of CD increases as goes down. However, urea is able to get out on distal end. It moves towards and reenters tubular system at ascending loop.
In process it manages to redirect the flow of interstitial NaCl back towards blood.
RECYCLING OF UREA SAVES NACL...from being ****** out.

Front 44

1. 90% of biocarbonate (HCO3-) is reabsorbed in ________. Reabs. motivated by secretion of ______ into tubular lumen.

2. Diffuses easily thru _______membrane as CO2.

3. Bicarbonate returns to blood via ______ together with Na+

Back 44

1. 90% of biocarbonate (HCO3-) is reabsorbed in PROXIMAL tubule. Reabs. motivated by secretion of [H+] into tubular lumen.

2. Diffuses easily thru APICAL (LUMINAL) membrane as CO2;
H+ (not sure about relationship there) <- maybe b/c doesn't form CO2 unless H+ binds to bicarb (HCO3-)

3. Bicarbonate returns to blood via symport together with Na+

Front 45

Bulk [flow] takes place in ______ and ______.

Back 45

PT and LoH

(mostly PT - 2/3 H2O and Na+, 100% of glucose and amino acids)

Front 46

Strong acid dissociates ______ in solution into H+ and an anion. This anion is called ______.

Back 46

Strong acid dissociates almost completely into H+ & anion; anion is called a [conjugated base]

In aqueous solution almost all H+ is dissociated, and only if H+ conc. increases(added) then is H+ forced back into binding.

Front 47

If acid accumates and pH drops, which form becomes more prevalent (associated or dissociated)

Back 47

reaction moves to left

more H+ means more substrate for HCO3- to bind to

Front 48

Phosphate Buffers are usually in blood or inside cells?

Back 48

not in blood; prevalent inside cell

Front 49

RPF (mL/min) / 1 - HCT
tell you what?

(check this)

Back 49

basically this is just formula for converting plasma clearance rate (ml/min) to blood clearance rate (ml/min)

need to know the hematocrit (percentage of blood which is cells or not plasma)

helps to know RPF

RPF = urine conc x urine flow rate / plasma conc

Front 50

Renin release from JG cells is stimulated by ? (name three primary stimuli)

Back 50

Release is stimulated by:
1. sympathetic activation by B1
2. renal artery HYPOTENSION
3. decreased Na+ delivery to distal tubules of the kidney.

FYI: remember decr. BP & volume = leads to reduced GFR, reduced water and NaCl loss into urine.

Front 51

Renin stimulates release of ___ from blood and tissues.

Back 51

Renin stimulates the formation of ANGIOTENSIN-1 in blood and in tissues (A1 then converted to A2 in lungs and other tissues)

Front 52

Angiotensin II (A2) has many functions:
1. stimulates the release of ___ from adrenal cortex

2. Stimulates release of ___ from posterior pituitary gland

Back 52

1. Angiotensin II stimulates release of ALDOSTERONE from adrenal cortex.
2. Stimulates release of (ADH) from posterior pituitary

Front 53

Which hormone also has following affects:
3. Stimulates thirst centers within the brain (polydipsia)
4. Facilitates norepinephrine release from sympathetic nerve endings, enhancing sympathetic (adrenergic) effects

Back 53

Angiotensin II --> polydipsia, NOR release

in addition to aldersterone and ADH...

Front 54

ADH is also known as ?

Back 54

ADH = vasopressin

Front 55

ADH released from ?

Back 55

ADH is released from posterior pituitary gland

Front 56

ADH stimulates? function?

Back 56

Vasopressin (ADH) from posterior pituitary, increases fluid retention by the KIDNEYS.

Front 57

what 2 things stimulate the adrenal cortex to make aldosterone?

Back 57

- ATII
- hyperkalemia

Front 58

what does aldosterone stimulate?

Back 58

stimulates NaK ATPase pump
- retain Na
- secrete K

...Aldosterone is a SODIUM SAVER...remember A-S-S

Front 59

For more Renin-angiotensin-aldersterone system info...

http://www.cvphysiology.com/Blood%20Pressure/BP015.htm

Back 59

http://www.cvphysiology.com/Blood%20Pressure/BP015.htm

Front 60

What is end result of A2 induced norepinephrine release on systemic BP?

Back 60

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