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RENAL > 3 – Renal Blood Flow and Regulation > Flashcards

3 – Renal Blood Flow and Regulation Flashcards

1
Q

Kidneys vs. brain blood flow and oxygen consumption:

A

Kidneys:
-7x more blood flow: due to reabsorption processes
-use twice as much oxygen (per mass of tissue)

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2
Q

Why do kidneys require a lot of oxygen?

A

-for active reabsorption of sodium
-Ex. if GFR reduces, less sodium reabsorption is needed=less oxygen is required

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3
Q

What in general does renal blood flow depend on?

A

-pressure gradient across the renal vasculature
>arteriole pressure (+)
>venous pressure (-)

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4
Q

Total resistance of tissue:

A

-small arteries and arterioles increase the resistance to blood flow
*contribute to pressure gradient

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5
Q

Renal pressure gradient is estimated as (equation):

A

=(renal artery P – renal vein P) divided by (total renal vascular resistance)

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6
Q

Renal artery pressure equals:

A

-general pressure (=~100mmHg)

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7
Q

Renal vein pressure equals:

A

-3-4mmHg

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8
Q

Total renal vascular resistance is due to:

A

-small arteries and arterioles increase the resistance to blood flow
*contribute to pressure gradient

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9
Q

What are the 3 main determinants of renal vascular resistance?

A
  1. Interlobular arterioles: 16% reduction in P
  2. Afferent arterioles: 26% reduction in P
  3. Efferent arterioles: 43% reduction in P
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10
Q

What are some factors that can affect renal vascular resistance?

A

-sympathetic NS
-hormones and autacoids

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11
Q

Glomerular hydrostatic pressure:

A

-important factor in controlling GFR
*changes in it correlate with GFR

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12
Q

Sympathetic NS:

A

-innervation to all renal vessel
-less critical for normal physiological changes
-important under pathological conditions

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13
Q

What causes activation of the sympathetic NS in the kidneys?

A

-severe conditions
>hemorrhage
>brain ischemia

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14
Q

What happens when sympathetic NS is activated?

A

-vasoconstriction
-increased renal total vascular resistance
-reduced renal blood flow
*restores blood volume and prevents loss of water and electrolytes

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15
Q

What are the main hormones that affect renal blood flow?

A

-E
-NE
*less critical for normal physiological changes
*more important for pathological conditions (ex. hemorrhage)

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16
Q

What does E and NE do in the kidneys?

A

-constriction of afferent and efferent arterioles
-reduction of renal blood flow and GFR

17
Q

What determines the concentrations of NE and E?

A

-activation of sympathetic NS

18
Q

When is endothelin released?

A

-damage to renal endothelial cells (and other tissues)
*acts as a vasoconstrictor=reduces GFR

19
Q

What does endothelin do when there is tissue damage?

A

-reduces blood flow and blood loss

20
Q

What are some pathological conditions where endothelin is release?

A

-toxemia
-acute renal failure
-chronic uremia

21
Q

Angiotensin II:

A

-work locally and as a circulatory hormone
*constricts efferent arterioles

22
Q

When is Ang II released?

A

-volume depletion or reduced arterial pressure

23
Q

What happens when there is volume depletion or reduced arterial pressure?

A

-GFR is reduced to maintain water and electrolytes=fewer waste products are removed

24
Q

What does constriction of efferent arterioles by Ang II do?

A

-increases hydrostatic pressure of glomerular capillaries=increases GFR=more waste products are removed under a LOW arterial pressure condition
-reduces pressure in peritubular capillaries=facilitates reabsorption process as less water and Na is lost

25
Q

Endothelial-derived NO:

A

-released by endothelial cells
-vasodilator
-increases GFR (reduces resistance)
>important for excretion of Na and water

26
Q

What can damage to epithelial cells and reduced NO production lead to?

A

-hypertension

27
Q

What are some other vasodilators?

A

-prostaglandins
-PGE2 and PGE1
-bradykinin
*autocoids

28
Q

Autocoids:

A

-work on the cells close by

29
Q

What do the vasodilator autocoids do?

A

-increase GFR (not critical under physiological conditions)
-reduce vasoconstriction effect of Ang II on AFFERENT arterioles
>so that Ang II only works on EFFERENT arterioles

30
Q

What is the purpose of autoregulation of renal blood flow?

A

-to maintain GFR and excretion of water and solutes in spite changes in arterial P

31
Q

What are the 2 main mechanisms involved in autoregulation of renal blood flow?

A
  1. Autoregulation for maintaining GFR (tubuloglomerular feedback and myogenic autoregulation)
  2. Glomerulotubular balance mechanism to increase tubular reabsorption
32
Q

Tubuloglomerular feedback for regulation of GFR:

A

-based on Na-Cl and juxtaglomerular complex structure
-includes 2 responses

33
Q

2 responses of tubuloglomerular feedback:

A

-afferent arteriolar feedback
-efferent arteriolar feedback

34
Q

Macula densa:

A

-specialized cells in distal tubules
-located closed to juxtaglomerular cells which surround both afferent and efferent arterioles

35
Q

Afferent and efferent arteriolar feedback example when BP is less than normal: (opposite is true for when BP is more than normal)

A

-decrease GFR=less volume in tubules=flow in tubule will be slower=more time to reabsorb Na-Cl
-when reaches distal tubule, macula densa cells sense low Na-Cl and that GFR is low
-send signals to afferent arterioles to dilate them=increases hydrostatic P and increase GFR
-sends signals to increase renin release from juxtaglomerular cells (ang I +ang II)=constricts efferent arterioles=increases glomerular hydrostatic pressure and GFR

36
Q

Individual blood vessels during increased arterial pressure:

A

-are able to restrict the stretching
*myogenic autoregulation

37
Q

Myogenic autoregulation of renal blood flow and GFR: mechanism

A
  1. Stretch of the vascular wall leads to transfer of extracellular Ca2+ into smooth muscles cells
  2. Leads to contraction of the cells which further reduces the stretch of vascular wall=prevents increased renal blood flow and GFR
    *important to prevent renal damage in cases of sudden increases in BP

RENAL (15 decks)

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