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Physiology > Glomerular Filtration & Renal Blood Flow > Flashcards

Glomerular Filtration & Renal Blood Flow Flashcards

1
Q

Excretion Rate: Three renal processes

A

1.)Glomerular filtration From glomerular capillaries to Bowman’s capsule
2.)Tubular reabsorption:From renal tubules to
peritubular capillaries
3.) Tubular secretion From peritubular capillaries to renal tubules
Excretion =Filtration – Reabsorption + Secretion

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2
Q

why high filtration rate

A

llows rapid removal of waste products  These substances depend on filtration for adequate
removal (i.e. not reabsorbed or secreted) Allows multiple passes of the blood volume through the kidneys each day

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3
Q

daily GFR

A

180 L/day versus 3 to 4 liters of plasma volume  Allows complete filtering of plasma volume 6 times each day Allows rapid and precise control of body fluid volume and composition

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4
Q

filtration rate=

A

GFR / Renal Plasma Flow
≈ 20%
 Each minute 20% of the plasma flowing through the kidneys is filtered

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5
Q

normal reabsorption daily

A

≈ 178.5 Liters/day (123 mls/minute)

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6
Q

Normal urine output daily

A

180 – 178.5 ≈ 1.5 Liters/day

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7
Q

Normal urine output per minute

A

125 -123 ≈ 2 mls/minute

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8
Q

glomerular Capillary Membrane is different from reg. capillaries how?

A

lters significantly more volume than normal capillaries – Thicker but more porous Three major layers (not 2) Endothelial cell layer Basement membrane layer Epithelial cell layer
Podocytes: surround outer surface of basement membrane

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9
Q

Endothelial layer

A

perforated by thousands of fenestrations (small holes)

 Protein passage prevented by negative charge on surface of endothelial cells

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10
Q

Basement membrane

A

allows movement of water and small solutes

Protein passage prevented by proteoglycan mesh and negative charge

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11
Q

Epithelial layer

A

not continuous
 Slit pores present between adjacent podocytes – allow free movement of water and small solutes
 Negative charge of surrounding epithelial cells hinders protein filtration
 Overall pore size approximately 8 nanometers (80 angstroms)

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12
Q

Filterability of 0.75 means

A

iltered 75% as quickly as water

 Filtrate concentration < plasma concentration

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13
Q

Filterability of 1.0 means

A 
freely filtered (at the same rate as water)
 Concentration in filtrate will equal plasma
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14
Q

Dextrans

A

Polysaccharidesthat can be made with specific charges. polycationic dextran more filterable than polyanionic because of repelling of negative charges from molecule and pore

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15
Q

In some renal diseases, the negative charge of basement membrane is lost before any histological changes are seen and will cause

A

appearance of albumin in urine is an early indicator

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16
Q

GFR=

A

Kf x Net filtration pressure. Kf is the glomerular capillary filtration coefficient. Net filtration pressure ≈ 10 mmHg

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17
Q

Promotes filtration

A

Glomerular hydrostatic pressure (60 mmHg)

Bowman’s capsule oncotic pressure (0 mmHg) (factor with disease)

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18
Q

Inhibits filtration

A

Glomerular oncotic pressure (32 mmHg)  Bowman’s capsule hydrostatic pressure (18 mmHg)

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19
Q

Glomerular Capillary Filtration Coefficient

A

Affected by overall hydraulic conductivity and surface area of the glomerular capillaries
 Not able to measure directly  Kf = GFR / Net filtration pressure
Kf = 125 mls/min / 10 mmHg = 12.5 mls/min/mmHg  Kf = 4.2 mls/min/mmHg/100 grams of tissue

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20
Q

Normal Kf other capillaries=

A

0.01 mls/min/mmHg/100 gm

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21
Q

Filtration Coefficient and GFR

A

Direct positive relationship
 Usually not part of day-to-day control of GFR
 Can be affected by disease  Decreasing number of function glomerular capillaries
(decreased surface area)
 Increasing thickness of membrane (decreased hydraulic conductivity)
 Hypertension & diabetes mellitus

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22
Q

Factors Affecting GFR

A

Colloid Osmotic Pressure & Filtration Fraction Hydrostatic Pressure

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23
Q

Oncotic Pressure – Glomerulus

A

Increased glomerular oncotic pressure = Decreased GFR

 Decreased glomerular oncotic pressure = Increased GFR

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24
Q

As blood passes through glomerulus plasma oncotic pressure will increase

A

≈ 20%
 Approximately 20% of fluid is filtered producing increased [protein]
 Plasma oncotic pressure ≈ 28 mmHg entering glomerulus
 Glomerular oncotic pressure ≈ 36 mmHg as blood leaves glomerulus
[32 mmHg average]

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25
Q

Factors Affecting Glomerular Oncotic Pressure

A

Plasma protein concentration of arterial blood  Increased plasma protein concentration will increase
glomerular oncotic pressure which will decrease GFR  Fraction of plasma being filtered (filtration fraction)
 Increased filtration fraction means more plasma is being filtered from each ml of blood in the glomerulus
 As blood is concentrated the oncotic pressure of blood remaining in the glomerulus increases which will decrease GFR

26
Q

Filtration Fraction and GFR

A

Filtration fraction = GFR / RBF
 A decrease in RBF (no initial change in GFR) will increase the filtration fraction thus producing a decrease in GFR
 Changing RBF with constant glomerular hydrostatic pressure thus has an effect on GFR
 Increased RBF – Decreased Fraction – Decreased glomerular oncotic pressure – Increased GFR

27
Q

HYDROSTATIC PRESSURE

A

Increased pressure = Increased GFR  Decreased pressure = Decreased GFR
 Primary means of controlling GFR  Arterial pressure
 Increased MAP = Increased GFR [Buffered by autoregulation of flow to keep consistent glomerular pressure]
 Afferent arteriole resistance  Efferent arteriole resistance

28
Q

Afferent Arteriole Resistance

A

Increased constriction = Decreased pressure = Decreased GFR
 Decreased constriction = Increased pressure = Increased GFR
 As constriction increases, RBF also decreases.  But GFR decreases at a faster rate

29
Q

Efferent Arteriole Resistance initially

A

Increased constriction = Increased pressure = Increased GFR
 Decreased constriction = Decreased pressure = Decreased GFR
 But not as simple as it appears!!

30
Q

efferent arteriole resistance as constriction increase

A

As constriction increases, RBF will decrease while glomerular pressure increases
 INITIALLY the change in glomerular pressure has more effect than the decrease in RBF which produces an overall increase in GFR.
 [Increase in glomerular pressure greater than decrease in RBF]
 BUT as constriction continues to increase the change in filtration fraction begins to play a role:
 Filtration fraction increases (decreased blood flow, increased GFR) which results in higher glomerular colloid oncotic pressure which decreases GFR
 When effect of the increase in glomerular oncotic pressure exceeds the effect of the increase in hydrostatic pressure, the GFR will decrease

31
Q

Hydrostatic Pressure – Bowman’s Capsule

A

Increased hydrostatic pressure = Decreased GFR  Decreased hydrostatic pressure = Increase GFR
 Normally does not play a primary role in controlling GFR
 Obstruction of urinary tract
 Could produce big increase in pressure with big decrease in GFR

32
Q

decrease in Kf (glomerular filtration coefficient) will cause

A

decrease in GFR. possibly caused by renal disease, diabetes mellitus, hypertension

33
Q

increase in PB (Bowman’s hydrostatic pressure) will cause

A

decrease in GFR. caused by urinary tract obstruction (kidney stones)

34
Q

increase in sigma G (glomerular capillary colloid osmotic pressure) will cause

A

decrease in GFR. caused by a decrease in BF or an increase in proteins

35
Q

decrease in PG (glomerular hydrostatic pressure) will cause

A

decrease in GFR

36
Q

decrease in AP

A

decrease in PG but only has small effect due to autoregulation

37
Q

decrease in RE

A

decrease in PG. drugs that block angiotensin 2 formation

38
Q

increase in RA

A

decrease in PG. increased sympathetic activity. vasoconstrictor hormones like nore, epi, or endothelin

39
Q

Regulation of RBF closely linked to

A

control of GFR and excretion

40
Q

RBF provides flow for

A

basic metabolic needs of kidneys and excess flow for plasma filtration

41
Q

Renal O2 consumption is

A

2x that of the brain BUT blood flow is 7x

42
Q

Most of O2 consumed supports

A

sodium reabsorption – consumption directly related to rate of sodium reabsorption

43
Q

Determinants of RBF

A

(Renal artery pressure – Renal vein pressure) / Total renal resistance
 Arterial ≈ 100 mmHg; Venous ≈ 4 mmHg

44
Q

Percentage of renal vascular resistance

A

 Afferent arterial ≈ 26%  Efferent arterial ≈ 43%  Interlobar, arcuate, interlobular arteries ≈ 16%
 Account for 85% total renal resistance

45
Q

Resistance of these three areas controlled

A

by sympathetic
nervous system, hormones, local control within kidneys
 Increased resistance tends to reduce RBF
 Decreased resistance tends to increase RBF (assume no change in arterial or venous pressures)

46
Q

Flow Distribution Within Kidney

A

98 to 99% goes to renal cortex

 1 to 2% goes to renal medulla via the vasa recta  Key part of ability to concentrate urine

47
Q

Effect of Sympathetic Activation

A

All vessels receive sympathetic innervation  Strong activation – Constriction
 Decrease RBF and GFR  Mild to moderate activation (moderate decrease in
BP with corresponding baroreceptor response)  Little effect on RBF or GFR
 Most important when body faced with life threatening problem
 Severe hemorrhage  Healthy normal person – very little effect

48
Q

Hormonal Effect on Epi, Norepi, Endothelin

A

Epinephrine and norepinephrine  Effect similar to effect of sympathetic nervous system
 Endothelin
 Released by damaged vascular endothelial cells of kidneys and other tissue – play role in hemostasis??
 Concentration increased during toxemia of pregnancy, acute renal failure, chronic uremia
 Powerful vasoconstrictor

49
Q

Hormonal Effect of Angiotensin II

A

Potent vasoconstrictor that is normally circulating and is produced locally
 All renal vessels contain receptors but preglomerular vessels show weak if any response because of simultaneous release of vasodilators such as nitric oxide and prostaglandins
 Strong effect on efferent arterial producing increased glomerular pressure AND decreased renal blood flow
 Helps reduce decrease in GFR during times of decreased MAP and/or volume depletion
 Enhanced tubular reabsorption because of decreased flow thru peritubular capillaries

50
Q

Hormonal Effect of Nitric Oxid

A

Renal endothelial cells release a basal level that helps maintain dilation of renal vessels
 Giving nitric oxide inhibitor  Increases renal vascular resistance  Decreases GFR & urinary excretion of sodium
 If continued will result in an increase in MAP due to the increased sodium levels

51
Q

Hormonal Effect of Bradykinin & Prostaglandins

A

Potent vasodilators
 Tend to increase RBF and GFR
 Do not appear to have major impact during normal conditions
 May dampen effect of sympathetic nerves and angiotensin II
 May help prevent excessive decreases in RBF and GFR
 Inhibited by administration of nonsteroidal anti- inflammatory agents

52
Q

Autoregulation of RBF & GFR

A

 Mechanisms are intrinsic to the kidneys  Function without systemic or neural influence
 Purpose is to maintain NORMAL GFR and allow control of renal excretion of water and solutes
 Prevents big changes in water / solute excretion with normal changes in blood pressure
 Decreasing MAP to 75 mmHg or increasing to 160 mmHg results in a small change in GFR (<10% change)
 RBF not as well controlled as GFR

53
Q

What Would Happen If No Autoregulation

A

 Increased MAP 100 to 125 mmHg  GFR would go from 180 L/day to 225 L/day
 If reabsorption then remained constant:  225 – 178.5 = 46.5 L/day of urine output  Would quickly deplete the circulating blood volume
 Large increase in urine output prevented by
 Autoregulation
 Changes in tubular reabsorption  Adaptive tubular mechanisms that produce increase in reabsorption
with an increase in GFR  Glomerulotubular balance
 But urine output and solute excretion DOES increase with an increase in MAP
 Pressure diuresis and pressure natriuresis

54
Q

Tubuloglomerular Feedback Mechanism

A

Links autoregulation of GFR and RBF to the amount of NaCl entering the distal tubule
 Regulates RBF and GFR in parallel
 GFR regulation rather than RBF regulation plays larger role in maintaining constant delivery of NaCl to distal tubule
 Components  Afferent arteriole feedback mechanism  Efferent arteriole feedback mechanism  Juxtaglomerular complex

55
Q

Juxtaglomerular Complex - Structure

Macula densa cells

A

 Epithelial cells located initial part of distal tubule
 In contact with portions of afferent & efferent arterioles
 Contain secretory Golgi apparatus  Sense changes in NaCl
concentration in the tubular fluid

56
Q

Juxtaglomerular cells

A

Surround afferent arteriole where it enters the glomerulus
 Surround efferent arteriole where it leaves glomerulus
 In contact with portion of distal tubule that contains macula densa
 Major storage site for renin

57
Q

Juxtaglomerular Complex - Operation

A

Believed that macula densa monitors amount of volume delivered to distal tubule via NaCl concentration
 As GFR decreases  Flow rate through Loop Henle also decreases  Reabsorption of Na+ and Cl- in loop increases  Concentration Na+ and Cl- at macula densa decreases  Decreased concentration elicits response from macula densa

58
Q

Response from macula densa has two effects

A

Dilationofafferentarteriole
 Results in an increase in glomerular hydrostatic pressure
 Stimulation of increased renin release from juxtaglomerular cells
 Results in an increased constriction of efferent arteriole which produces an increase in glomerular hydrostatic pressure
 Prevents major changes in GFR between MAPs of 75 to 160 mmHg

59
Q

Myogenic Autoregulation

A

An increase in MAP will cause an increase in smooth muscle contraction especially of small arterioles
 MAP increases which cause the vessel walls to stretch thus increasing wall tension. The increased stretch results in movement of additional calcium into the smooth muscle cells which increases the overall level of contraction
 Not sure how important this mechanism is for the kidneys, but it has been shown that the afferent arterioles show a strong myogenic response to sudden increase in arterial pressure
 Result of increased afferent constriction is a reduction in RBF (due to increased resistance) and a decrease in GFR (due to decreased glomerular hydrostatic pressure)

60
Q

Problems With Juxtaglomerular Feedback

A

eedback mechanism designed to maintain consistent delivery of NaCl to the distal tubule
 Any problem that increases NaCl reabsorption in the proximal tubule will trigger the feedback mechanism
 High protein intake
 Higher than normal amino acid concentration in the blood – Sodium and amino acid reabsorption linked, so an increase in amino acid reabsorption results in an increase in sodium reabsorption and stimulation of the feedback mechanism (20 to 30% increase in GFR 1 to 2 hours after eating a high-protein meal
 Increase in blood glucose
 Again, glucose reabsorption tied to sodium reabsorption – As concentration of glucose in the blood increases, glucose and sodium reabsorption also increase thus stimulating the feedback mechanism which ultimately results in an increase in GFR

Physiology (27 decks)

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