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SMP - Renal > Lecture 7 - Regulation of Renal Hemodynamics > Flashcards

Lecture 7 - Regulation of Renal Hemodynamics Flashcards

1
Q

Does the process of glomerular filtration utilize O2?

A

NOPE

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2
Q

Why does the kidney use O2?

A

Active reabsorption

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3
Q

Does the blood flow to the kidney exceed its O2 needs?

A

BY FAR

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4
Q

What is the relationship between higher renal blood flow and O2 consumption?

A

Higher blood flow => higher GFR => higher rate of active reabsorption => higher O2 consumption

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5
Q

Equation for flow rate through an organ?

A

Q = ΔP/R

ΔP = pressure differential through the capillary bed

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6
Q

Resistance in the kidney?

A
  1. Afferent arteriole = RA
  2. Efferent arteriole = RE

RT = RA + RE

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7
Q

How does pressure vary through the efferent arteriole?

A

Decreases

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8
Q

Describe hydrostatic and oncotic pressures in the peritubular capillaries. What does this facilitate?

A

Higher oncotic pressure than hydrostatic because of the filtration of plasma through the glomerulus => facilitates reabsorption

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9
Q

How is RPF affected by increasing mean renal arterial pressure? What is this called? What does this mean for GFR?

A

Relatively constant (very slight increase) from 80 to 180 mmHg and increases outside of that range => MYOGENIC (AUTO)REGULATION: renal arterioles constrict reflexively in response to increased pressure to increase resistance

Same for GFR

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10
Q

Why are there limits to the kidney autoregulation of blood flow?

A
  • Past 180 mmHg: renal arteriole is maximally vasoconstricted
  • Before 80 mmHg: renal arteriole is maximally vasodilated
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11
Q

Describe autoregulation of blood flow. Purpose?

A

Increase in transmural pressure of the arteriole/capillary sphincter => stretched smooth muscle => depolarization of smooth muscle => contraction => decreased vessel diameter (or opposite mechanism with hyperpolarization)

Purpose: ability to normalize flow in the face of fluctuating transmural pressure to keep local flow relatively constant

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12
Q

Effect of afferent arteriole vasoconstriction on glomerular hydrostatic pressure?

A

Decreases it

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13
Q

Effect of efferent arteriole vasoconstriction on glomerular hydrostatic pressure?

A

Increases it

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14
Q

Effect of efferent arteriole vasodilation on glomerular hydrostatic pressure?

A

Decreases it

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15
Q

Effect of afferent arteriole vasodilation on glomerular hydrostatic pressure?

A

Increases it

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16
Q

Constriction of afferent arteriole:

  1. Effect on renal plasma flow?
  2. Effect on GFR?
  3. Effect on filtration fraction (GFR/RPF)?
  4. Oncotic pressure in peritubular capillary compared to normal?
A
  1. Decrease
  2. Decrease
  3. No change
  4. No change
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17
Q

Dilation of afferent arteriole:

  1. Effect on renal plasma flow?
  2. Effect on GFR?
  3. Effect on filtration fraction (GFR/RPF)?
  4. Oncotic pressure in peritubular capillary compared to normal?
A
  1. Increase
  2. Increase
  3. No change
  4. No change
18
Q

Constriction of efferent arteriole:

  1. Effect on renal plasma flow?
  2. Effect on GFR?
  3. Effect on filtration fraction (GFR/RPF)?
  4. Oncotic pressure in peritubular capillary compared to normal?
A
  1. Decrease
  2. Increase
  3. BIG increase
  4. Increase
19
Q

Dilation of efferent arteriole:

  1. Effect on renal plasma flow?
  2. Effect on GFR?
  3. Effect on filtration fraction (GFR/RPF)?
  4. Oncotic pressure in peritubular capillary compared to normal?
A
  1. Increase
  2. Decrease
  3. BIG decrease
  4. Decrease
20
Q

Dilation of afferent arteriole + constriction of efferent arteriole:

  1. Effect on renal plasma flow?
  2. Effect on GFR?
  3. Effect on filtration fraction (GFR/RPF)?
  4. Oncotic pressure in peritubular capillary compared to normal?
A
  1. No change
  2. BIG increase
  3. BIG increase
  4. BIG increase
21
Q

What endogenous hormone will dilate the afferent arteriole and constrict the efferent arteriole?

A

ANP

22
Q

Do the vasomotor effects of ANP extend beyond the renal arteries?

A

NOPE

23
Q

Effects of angiotensin II on renal blood flow?

Filtration fraction in particular? Explain how it works in detail.

A

Decrease in blood volume => kidney secretes renin => renin converts angiotensinogen (from liver) to angiotensin I => ACE (from lungs endothelium and every other endothelial cell) converts angiotensin I to II =>

  1. Angiotensin II first constricts the afferent arteriole, which decreases RPF and GFR
  2. Angiotensin II then constricts the efferent arteriole, which increases GFR slightly (not back to its normal value though), and further decreases RPF + decrease GFR further accentuated by the effect of angiotensin II on the size of the filtration slits leading to decreased filtration surface area
  3. Overall, there is a large decrease in RPF and a slight decrease in GFR leading to an INCREASE in filtration fraction

=> increases GFR/RPF => increases peritubular oncotic pressure => increased BP and intravascular volume

24
Q

What does the oncotic pressure in the peritubular capillaries depend on?

A

GFR/RPF

25
Q

Constriction of afferent arteriole + constriction of efferent arteriole:

  1. Effect on renal plasma flow?
  2. Effect on GFR?
  3. Effect on filtration fraction (GFR/RPF)?
  4. Oncotic pressure in peritubular capillary compared to normal?
A
  1. BIG decrease
  2. Decrease
  3. Increase
  4. Increase
26
Q

Other than through myogenic regulation, how else does the kidney regulate its blood flow? Explain how it works. What do we call this?

A

Macula densa cells!

Decreased tubular flow => macula densa senses it => MDCs trigger a response => rise in GFR in that same nephron (and vice versa with increased tubular flow)

Tubuloglomerular feedback

27
Q

Timing of the tubuloglomerular feedback and myogenic regulation? Importance of this?

A

Minute to minute

“Weak” system, that is completely overiden by systemic regulations, e.g. SNS, vasoactive blood hormones, etc.

28
Q

What are the 2 intrinsic feedback systems of GFR?

A
  1. Myogenic regulation

2. Tubuloglomerular feedback

29
Q

ANS innervation of kidneys?

A

Sympathetic ONLY

30
Q

Describe the effect of hemorrhage on the kidneys.

A

Decrease arterial pressure => decreased firing of carotid sinus and aortic arch baroreceptors => increased activity of renal sympathetic nerves => increased constriction of renal arterioles due to sympathetic nerves AND circulating catecholamines from the medulla => decreased RBF and GFR

31
Q

Describe the kidney secretion of renin. What do they all have in common? Purpose?

A

Secretion of renin into renal vein is stimulated by 3 factors:

  1. Decreased firing of baroreceptor in afferent arteriole
  2. Increased sympathetic activity on the afferent arteriole on beta adrenergic receptors
  3. Decreased tubular flow => macula densa senses it => MDCs trigger renin secretion

COMMON: impaired renal perfusion

Purpose: raise BP

32
Q

What happens if there is an athreosclerotic plaque in the renal artery?

A

Impaired renal perfusion => renin secretion

33
Q

What are the 2 prostaglandins made by the kidney? Are they actively/normally made in the kidney?

A

PGE 2 and PGI 2

NOPE

34
Q

What does PGI 2 stand for?

A

Prostacyclin

35
Q

Describe how prostaglandins regulation renal blood flow.

A

Increased activity of renal sympathetic nerves + increased plasma angiotensin II => increased renal prostaglandin synthesis and release => modulates the constriction by vasodilating the renal arterioles

36
Q

2 renal vasodilators?

A
  1. Prostaglandins

2. Low dose dopamine (so that only the kidneys dilate)

37
Q

Why is it hard to increase GFR by using vasodilators?

A

Because systemic vasodilators decrease BP => decrease renal blood flow

38
Q

Is renal arterial pressure the same as systemic arterial pressure?

A

YUP

39
Q

Purpose of autoregulation of RBF?

A
  1. Protect glomerular capillaries from hypertensive damage

2. Preserve healthy GFR

40
Q

Which nephron segment a major tubular site of action of Ang II?

A

PCT

SMP - Renal (20 decks)

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