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Kathleen's Renal I > Renal Blood Flow and Glomerular Filtration > Flashcards

Renal Blood Flow and Glomerular Filtration Flashcards

1
Q

Describe the 3-layered structure of the glomerular capillary filtration membrane and list blood components that are restricted from filtration by each layer.

A

Membrane:

  1. Fenestrated capillary endothelium - highly permeable to water, dissolved solutes
    (keeps out cellular elements, platelets)
  2. Glomerular basement membrane - collagen, proteoglycans contain anionic (negative) charges
    (keeps out anions, small proteins)
  3. Podocyte epithelium - slit pores between podocytes restrict large molecules
    (large molecules, more proteins)
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2
Q

Define the ultrafiltration coefficient at the glomerular capillary, describe the membrane properties that contribute to it, and explain its role in determining GFR.

A

Ultrafiltration coefficient = Kf

Membrane properties:

  1. Hydraulic conductivity (Lp) of glomerular membrane (permeability or porosity of capillary wall)
  2. Surface area available for filtration (c. 2 m2)

GFR = Kf x Puf

Kf is a reflection of overall filtration of the glomerular membrane

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3
Q

Identify the components of the filtration barrier whose damage would result in hematuria and proteinuria.

A

Hematuria: blood in the urine
-happens as a result of breakdown of nephrins, podocytes, or fenestrated epithelium

Proteinuria: protein in urine

  • happens as a result of breakdown of glomerular basement membrane
  • can become quite damaged before pathology presents
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4
Q

Predict the changes in net filtration force that occur as blood travels along the glomerular capillary and hydrostatic pressure falls while colloid osmotic pressure increases.

A

Net filtration is proportional to glomerular capillary hydrostatic pressure

Net filtration is inversely proportional to colloid osmotic pressure
- oncotic pressure is higher in efferent arteriole, but still favors filtration

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5
Q

Given the capillary and Bowman’s space hydrostatic and oncotic pressures, calculate the net filtration force at the glomerular capillaries and predict changes in glomerular filtration by increases or decreases in any of these pressures.

A

Use this equation:

Puf = Pgc - (Pbc+ Pigc)

Determined by hydrostatic and colloid osmotic pressures in glomerulus, and hydrostatic pressure of Bowman’s capsule.
- Bowman’s capsule shouldn’t have much oncotic pressure

Increasing Pgc increases filtration
Increasing Pbc or Pigc decreases filtration

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6
Q

What can alter GFR?

A

Alter Kf - change surface area or conductivity

  • mesangial cell contraction
  • disease states

Puf - changes Pgc

  • renal artery BP
  • afferent arteriolar pressure
  • efferent arteriolar pressure
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7
Q

How do glomerular mesangial cells alter Kf?

A

Glomerular mesangial cells (M) located within glomerular capillary loops.

Contraction of mesangial cells shortens capillary loops, lowers Kf and, thus lowers GFR.

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8
Q

What is a list of factors that decrease GFR?

A 
Decreased Kf
Increased Pb
Increased Pigc
Decreased Pgc (most GFR reg happens here for normal individuals)
Decreased arterial pressure
Increased afferent arteriole pressure
Decreased efferent arteriole pressure
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9
Q

What are the effects of afferent arteriolar constriction?

A

Afferent arteriolar constriction:
Greater pressure drop upstream of glomerular capillaries
PGC falls, which lowers GFR
Renal blood flow falls due to  resistance

Hydrostatic pressure of peritubular capillaries decreases

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10
Q

What are the effects of efferent arteriolar constriction?

A

Efferent arteriolar constriction:
Pooling of blood in glomerular capillaries
Increased PGC increases GFR

Hydrostatic pressure of peritubular capillaries decreases

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11
Q

What is renal blood flow increased by?

A

Decreased efferent arteriole pressure

Decreased afferent arteriole pressure

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12
Q

What happens to GFR, RBF, and Pgc when afferent arteriolar resistance goes up?

A

They decrease

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13
Q

What happens to GFR, RBF, and Pgc when efferent arteriolar resistance goes up?

A

Pgc and GFR increase at first, then decrease with added resistance

RBF goes down, which eventually dictates the falling GFR

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14
Q

What is RBF? What is it important in? What regulates it?

A

Important in regulation of body fluid volume and solute concentration
Regulated by several mechanisms in order to control GFR
Oxygen consumption of renal tissue is higher than that of the brain
Related to high rate of active Na+ reabsorption (drives Na+/K+ ATPase)

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15
Q

What is the formula for RBF?

A

RBF = renal artery pressure-renal vein pressure

Divided by

total renal vascular resistance

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16
Q

What is renal blood flow controlled by?

A

Vascular resistance to RBF is primarily determined by afferent and efferent arterioles
Controlled by sympathetic nervous system (NE) and various hormones along with internal (myogenic, TG feedback) control mechanisms
GFR is strictly regulated over a MAP range between 80 and 170 mmHg via a process called autoregulation
Cortex receives most RBF, medulla receives less (vasa recta)

17
Q

Define autoregulation and describe its role in maintenance of RBF, GFR.

A

The ability of the kidneys to maintain GFR and renal blood flow at relatively constant rates, despite marked changes in arterial blood pressure.

Primary function in most tissues is to deliver oxygen/nutrients and remove waste products of metabolism

Primary function in the kidneys is to maintain constant GFR and precisely control excretion of water and solutes

Autoregulation: control of GFR over a MAP range of 80-170 mm Hg

18
Q

What are some mechanisms that cause vasoconstriction?

A

Sympathetic nervous system activation decreases GFR via constriction of the renal arterioles (afferent»efferent), decreasing RBF and GFR

Endothelin is a peptide hormone (autacoid) released by damaged vascular endothelial cells

Angiotensin II preferentially constricts efferent arterioles

19
Q

What are the effects of sympathetic stimulation on renal fraction?

A

Sympathetic nervous system activation

Diverts the renal fraction to vital organs
- Seems to be most important in reducing GFR during severe, acute disturbances (defense reaction, brain ischemia, hemorrhage, etc.)

20
Q

What are the endocrine effects of sympathetic innervation on the kidney?

A

SNS activation causes ↑ renin secretion by granular cells

Angiotensin II thus produced restores blood pressure (systemic vasoconstriction)

Angiotensin II promotes arteriolar constriction (efferent > afferent): raises blood pressure, may stabilize GFR (moderate Ang II)

21
Q

What are the effects of SNS activation on kidney function and resorption?

A

SNS activation ↑ Na+ reabsorption in proximal tubule, thick ascending limb (LOH), distal convoluted tubule, collecting duct

22
Q

What are the effects of angiotensin II?

A

Ang II is considered a circulating hormone as well as an autacoid

Receptors are present in all blood vessels of the kidneys

Afferent arterioles appear to be “protected” from the effects of Ang II, while efferent arterioles are highly sensitive to it

Aids in maintaining GFR in instances of pressure or volume depletion, helps to increase Na+ and H2O reabsorption

Stimulates aldosterone secretion and the thirst center

23
Q

What are mechanisms that promote vasodilation?

A

Endothelial-Derived Nitric Oxide

Prostaglandins and Bradykinin

24
Q

How does endothelial-derived nitric oxide work?

A

Endothelial-Derived Nitric Oxide

Vascular endothelial cells release NO, an important factor involved in normal vasodilation in the kidneys

Appears to be important in allowing the
kidneys to excrete normal amounts of Na+ and H2O

What would happen if you were to administer a drug that blocked NO - potential kidney collapse/renal failure

25
Q

What are the effects of prostaglandins and bradykinin?

A

Prostaglandins and Bradykinin
These are not of major importance in regulating GFR in normal conditions, but are extremely important in regulating the vasoconstriction caused by other mechanisms during situations like volume depletion (or after surgery)

26
Q

What is the effect of norepinephrine, epinephrine, and endothelin on GFR?

A

They decrease it

27
Q

What is the effect of ang II on GFR?

A

Prevents decrease

28
Q

What is the effect of endothelial-derived NO or prostaglandins on GFR?

A

The increase it

29
Q

What are 2 effects of autoregulation?

A

Autoregulation happens due to glomerulus being between 2 capillary beds

  1. protects glomerulus at times of high BP
  2. Protects GFR at times of low systemic BP
30
Q

What happens to urinary output with increased renal arterial pressure?

A

Would increase, but autoregulation keeps it within reasonable ranges

31
Q

What are some autoregulatory mechanisms?

A

Myogenic
Responds to increased systemic arterial pressure
Involves vascular smooth muscle cells

Tubuloglomerular feedback
Responds to increased OR decreased GFR
Involves macula densa cells, juxtaglomerular cells, extraglomerular mesangial cells

32
Q

What is the myogenic mechanism of autoregulation?

A

Mechanism to maintain constant RBF and GFR

Resistance of blood vessels to stretch when exposed to high arterial pressure

Vascular smooth muscle cells contract in response to stretch via movement of Ca2+ from ECF into cells
- Occurs within seconds

May be most important in protecting the kidney from hypertension-induced damage

33
Q

What is tubuloglomerular feedback?

A

Ensures constant delivery of NaCl to distal tubule and prevents changes in renal excretion

34
Q

How does tubuloglomerular feedback work?

A

Macula densa cells in the distal tubule detect changes in NaCl (volume is inferred) delivery

Macula densa cells communicate with juxtaglomerular cells in the afferent and efferent arterioles to affect resistance

A drop in delivery of NaCl (and therefore volume) to macula densa leads to:
- decreased resistance to blood flow in the afferent arterioles
- Increased renin release from the juxtaglomerular cells
(Ang II constricts the efferent arteriole&raquo_space;afferent arteriole)

35
Q

How does SNS react to tubuloglomerular feedback?

A

SNS activated by decreased volume and GFR, leading to afferent arteriolar constriction to conserve Na+ and water.

36
Q

What is the TGF response to increased GFR?

A

Constriction of afferent arteriole with a fall in GFR

- prevents limited reabsorptive capacity of collecting ducts from getting overwhelmed

37
Q

What chemical mediates response to TGF?

A

Adenosine mediates vasoconstriction in response to TGF in cases of elevated GFR

38
Q

What is glomerulotubular balance?

A

It is an adaptive mechanism of the renal tubules that cause them to increase their reabsorption rate whenever GFR rises.

39
Q

What will happen to GFR with most primary glomerular diseases?

A

Decrease it - usu due to loss of filtration surface, decreased Kf

Kathleen's Renal I (9 decks)

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