(05) - Renal Blood Flow Flashcards

1
Q

(Effects of Vasoconstriction)

What happens to…

  1. flow
  2. pressure upstream
  3. pressure downstream
  4. What is the value of sequential sphincters?
A
  1. decresed
  2. increases
  3. decreases

4.

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2
Q

place where you start seeing big change in pressure is at the afferent arteriole

A

he just talked about this for a spell

why is there such a reduction in pressure here (not sure where here is) but not here ( and again…)?

the main factor is that you have a pre and post glomerular filter - which allows you to maintain the pressure

in the second bed there aren’t two phincters which doesn’t allow for the maintentnce of pressure

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3
Q

note that efferent is smaller than afferent - therefore when it constricts it has a more profound effect on increasing resistance

A
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4
Q

(Effecot of Dual Sphincters)

1-2. What two things result from the presence of the two hincters?

  1. these pressure differences facilitate what in the glomeruli and what from the peritubular capillaries?
A
  1. glomerular capillary pressure much greater than in most capillaries elsewhere in the body
  2. peritubular capillary pressure is lower than in most capillaries elsewhere in the body
  3. formation of filtrate in glomeruli and reabsorption of fluid from peritubular capillaries
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5
Q

princiapl constrictors are sympathetic and angiotensin II

A
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6
Q

(Sympathetic NS and Catecholamines)

  1. sympathetic nerve fibers activate what on both afferent and efferent arterioloes? leads to what?
  2. many more a1 receptors on afferent or efferent?
  3. What would you predict the effect on RBF and GFR to be with SNS activation? answer the question…
A
  1. alpha1 receptors; vasoconstriction
  2. afferent
  3. A
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7
Q

(Angiotensin II (AT II))

  1. potent vasoconstrictor
  2. affects both AA and EA
  3. greter effect on which one?

answer the question

A
  1. efferent arteriole

answer is…..B

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8
Q

(Level of ATII Release Influences Relative Effects of ATII on AA vs EE)

(low levels of ATII)

  1. what happens to AA and EE?
  2. EA > AA, thus what happens to pressure in glomerular caps? what happens to GFR?

(As levels of ATII increase)

  1. what happens to AA and EA?
  2. EA <= AA, thus what happens to pressure in glomerular caps, thus what happens to GFR?
A
  1. both constrict
  2. thus increase in P in glomerular caps, thus get increasing GFR
  3. both constrict
  4. decreased pressure, decreased GFR

(for the most part we assume there are small levels of AT II)

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9
Q

Prostaglandins (PGE2 and PGI2)

(Vasodilator for both afferent and efferent arterioles)

  1. Activation of what two things also activates PG production?
  2. why does this make sense?
A
  1. SNS and ATII
  2. this is to prevent the reduction of blood flow to the kidney

advil is bad cause it messes up this protective vasodilation

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10
Q
A
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11
Q

(Dopamine)

  1. is a precurosor of what?

(Effects vary in different tissues and at different doses)

(at low doses)

  1. dilates what?
  2. constricts what?
  3. does what at high doses?

(Cat: no classical renal dopaminergic receptors)

A
  1. norepinephrine
  2. renal, cerebral, cardiac, and splachnic arterioles
  3. skeletal and cutaneous arterioles

(so it is very dose dependent)

  1. vasoconstricts renal arterioles
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12
Q

(Arterial BP and kidney function)

(kidney function remains relatively unaffected by changes in systemic arterial blood pressure)

  1. protects kidney function from what?
  2. protects glomerulus from what?
  3. what is this called?
A
  1. large and abrupt changes in systemic BP
  2. systemic pressure
  3. autoregulation

(there are changes in resistance that mitigate the changes in blood pressure) as pressure goes up resistance will have to go up - to keep the line level

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13
Q

(Autoregulation of RBF)

  1. autoregulation primarily controlled by what?

(theories explaining autoregulation)

(myogenic)

  1. what is the stimulus?
  2. what is the response?

(tubuloglomerular feedback)

A
  1. the afferent arteriole
  2. physical stretch of arterioloar wall
  3. opening smooth muscle Ca channels –> vasoconstriction
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14
Q
A
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15
Q

(Summary of Key Points)

  1. Is renal blood flow determined by functional or meatbolic needs?
  2. Renal cortical blood flow is unique because arterioles entering (afferent) and leaving (efferent) the glomerular capillaries contatin what?
  3. these two sphincters allows modulation of what and what?
A
  1. functional
  2. sphincters
  3. glomerular capillary blood flow and pressure
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16
Q

(Summary of Key Points)

  1. RBF is determined by the P at the renal artery and resistance of the AA and EA (note the AA and Ea are in series sor their resistance is addivitve)
  2. What are they key renal vasoconstrcitros?
  3. vasodilators?
A
  1. angiotensin II, sympathic NS (both have selective vascular affects)
  2. prostaglandins and dopamine
17
Q

(Symmary of Key Points)

  1. the kindeys have autoregulatory mechanisms that blunt changes in RBF and GFR in response to canges in what?
  2. Autoregulation involves modulation of renal afferent arterioloar resistance mediated by what two things?
A
  1. renal artery blood pressure
  2. myogenic mechanism and tubuloglomerular feedback
18
Q

(back tot he kitty)

so what happened?

A
19
Q
A
20
Q

(Starling Forces)

  1. movement of fluid from glomerular capillaries into the urinary space
  2. movement of interstical fluid into capillaries

3-5. Net flow across vessel wall depends on what three things?

A
  1. hydrostatic pressure on each side
  2. oncotic pressure on each side
  3. filtration coefficient of the vessel wall