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Tubular Reabsorption & Secretion Flashcards

1
Q

Excretion =

A

Filtration – Reabsorption + Secretion

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2
Q

Filtration

A

glomerulus

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3
Q

Reabsorption & Secretion:

A

Proximal tubule; loop of Henle; distal tubule; collecting tubule

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4
Q

Filtration rate =

A

GFR x Plasma concentration

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5
Q

Glucose concentration =

A

1 g/L

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6
Q

how much GFR daily

A

180 L

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7
Q

Filtration rate glucose =

A

(1 g/L) x ( 180 L/day) = 180 g/day

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8
Q

Kidneys has independent control

A

over exertion rate by changing appropriate reabsorption rate

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9
Q

GLUCOSE AMOUNT EXCRETED AND % REABSORBED

A

0 G/DAY 100%

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10
Q

BICARBONATE AMOUNT EXCRETED AND % REABSORBED

A

2 mEq/day >99.9 %

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11
Q

SODIUM AMOUNT EXCRETED AND % REABSORBED

A

150 mEq/day 99.4%

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12
Q

CHLORIDE AMOUNT EXCRETED AND % REABSORBED

A

180 mEq/day 99.1%

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13
Q

POTASSIUM AMOUNT EXCRETED AND % REABSORBED

A

92 mEq/day 87.8%

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14
Q

UREA AMOUNT EXCRETED AND % REABSORBED

A

23.4 g/day 50%

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15
Q

CREATININE AMOUNT EXCRETED AND % REABSORBED

A

1.8 g/day 0%

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16
Q

types of primary active transport for reabsorption

A

 Na-K ATPase  Hydrogen ATPase  H-K ATPase

 Ca ATPase

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17
Q

types of Secondary active transport: Co-

transport for reabsorption

A

 Sodium-glucose  Sodium-amino acids

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18
Q

types Secondary active transport: Counter-transport for reabsorption

A

 Sodium-hydrogen

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19
Q

Pinocytosis (requires energy) for tubular reabsorption

A

Proteins – once in cell broken down to component amino acids and amino acids reabsorbed

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20
Q

types Passive tubular reabsorption

A

 Osmotic movement of water

 Bulk flow into peritubular capillaries

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21
Q

how is sodium umped out of tubular cells into the interstitial spaces and Potassium pumped into tubular cells

A

 Na-K ATPase on basolateral sides of tubular epithelial cells
 Creates membrane potential -70 mV

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22
Q

how Sodium follows concentration gradient from tubular lumen into the tubular cells (diffusion down concentration & electrical gradients)

A

Brush board of proximal tubule luminal membrane creates huge surface area for diffusion (20x increase)

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23
Q

Sodium reabsorption also enhanced by

A

carrier proteins through luminal membrane

 Co-transport & counter-transport proteins

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24
Q

glucose reabsorption co transport mechanism tied to

A

sodium gradient from tubular lumen to interior of tubular cells
So efficient that usually removes all filtered glucose

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25
Q

Two luminal transporters for glucose reabsorption

A

SGLT2 and SGLT1
 90% glucose reabsorbed via SGLT2 in early part of proximal tubule
 10% reabsorbed in later part of proximal tubule via SGLT1

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26
Q

Glucose Reabsorption Two basolateral glucose transporters

A

GLUT2 and GLUT1. GLUT2 early stages of proximal tubule with GLUT1 in the later stages

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27
Q

type of transport GLUT2 AND GLUT 1 USE. Where does bulk flow go?

A

Passive facilitated transport down glucose concentration gradient. Bulk flow moves glucose from interstitial spaces into the peritubular capillaries

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28
Q

Amino Acid Reabsorption. Co-transport mechanism tied to ____ and the efficiency.

A

to sodium gradient from tubular lumen to interior of tubular cells
 So efficient that usually removes all filtered amino acids

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29
Q

amino acid Luminal co-transporter system pumps them where?

A

amino acids into the cells
 Amino acids diffuse out of the cells into the interstitial spaces
 Bulk flow moves the amino acids from interstitial spaces into the peritubular capillaries

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30
Q

Hydrogen Secretion Counter-transport mechanism tied to _____ and is located where?

A

Counter-transport mechanism tied to sodium gradient from tubular lumen to interior of tubular cells
 Sodium-hydrogen exchanger is located in brush boarder of the luminal membrane

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31
Q

Maximum Level of Active Reabsorption transport maximum:

A

Max amount of solute that can be reabsorbed (transport max transport)
 Occurs when tubular load (amount of solute delivered to tubule) exceeds transport capacity of carrier protein

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32
Q

Glucose Tmax =

A

375 mg/min

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33
Q

Glucose filtered load =

A

FR x [Glu] = 125 mls/min x 1 mg/ml = 125 mg/min

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34
Q

Threshold conc for glucose

A

(approx. 250 mg/dL) is concentration where glucose first appears in urine

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35
Q

why is Threshold conc for glucose less than t max?

A

Less than T max because each individual nephron is different – chart represents action of both kidneys so Tmax reached when ALL nephrons have reached their max

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36
Q

glucose transport max.

A

375 mg/min

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37
Q

phosphate transport max.

A

.10 mMol/min.

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38
Q

sulfate transport max.

A

.06 mM/min

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39
Q

amino acids transport max.

A

1.5 mM/min

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40
Q

urate transport max.

A

15 mg/min

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41
Q

lactate transport max.

A

75 mg/min

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42
Q

plasma protein transport max.

A

30 mg/min

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43
Q

Two excretion rates

A

Before secretion Tmax is reached the amount excreted is sum of amount filtered and amount secreted (steepest slope of excretion curve)
After secretion Tmax is reached rate of excretion parallels filtration rate (slope of excretion curve matches slope of filtration curve)

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44
Q

transport max for creatinine

A

16 mg/min

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45
Q

para-aminohippuric acid

A

80 mg/min

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46
Q

Gradient-Time Transport. rate of transport depends on

A

 Electrochemical gradient for solute  Membrane permeability for solute
 Time fluid containing solute remains in tubule  Transport rate inversely related tubular flow rate

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47
Q

Solute that is reabsorbed passively and some actively reabsorbed solute may not show

A

maximum rate of transport

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48
Q

Sodium Reabsorption: Proximal Tubule. Sodium does not show

A

a transport maximum even though it is actively reabsorbed

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49
Q

Sodium Reabsorption: Proximal Tubule. Capacity of Na-K ATPase usually

A

much greater than rate of net sodium reabsorption

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50
Q

Sodium Reabsorption: Proximal Tubule. Significant amount of transported sodium leaks back into the tubular lumen because of

A

 Permeability of tight junctions between cells  Forces controlling bulk flow of water & solute into peritubular capillaries

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51
Q

Sodium Reabsorption: Proximal Tubule. As plasma concentration of sodium increases

A

sodium concentration in proximal tubule increases and sodium reabsorption increases. A decrease in tubular flow rate will also increase sodium reabsorption

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52
Q

Sodium Reabsorption: Distal Tubule. Sodium reabsorption shows classic tubular max transport. why?

A

Capacity of Na-K ATPase does not exceed rate of net sodium reabsorption
 Minimal back leak of sodium into tubular lumen  Tighter (less permeable tight junctions) coupled transport of
much smaller amount of sodium  Aldosterone increases the Tmax level

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53
Q

Passive Reabsorption: Water driven by and affected by

A

 Driven by osmotic differences created by movement of solute (mainly sodium) from tubular lumen to the tubular interstitial spaces
 Affected by cellular permeability (cell membranes and tight junctions)  Increased permeability means increased reabsorption and decreased water excretion

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54
Q

Proximal tubule: permeability to water

A

Highly permeable

 Rapid movement so overall solute gradient across cell is minimal

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55
Q

solvent drag

A

water carries significant amount of sodium, chloride, potassium, calcium, magnesium because of high permeability

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56
Q

Loop of Henle (ascending loop) permeability to water

A

Low permeability Little movement of water even though there is a large osmotic gradient

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57
Q

Distal tubule / Collecting tubules / Collecting ducts: permeability to water

A

Variable permeability  Cellular permeability depends on presence of antidiuretic hormone (ADH)
 Permeability directly related to [ADH]
 Changing water permeability only affects amount of water reabsorbed not the amount of solute due to low solute permeability

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58
Q

Passive Reabsorption: Chloride relate to sodium diffusion, movement of water

A

Sodium diffusion into cells creates electrical gradient that pulls negative chloride ions into the cell
 Movement of water into cells concentrates chloride creating concentration gradient into cell
 Chloride also linked to co-transport mechanism with sodium across the luminal membrane

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59
Q

passive reabsorption urea: relate to water movement

A

Movement of water into cells concentrates urea creating concentration gradient into cell but urea not nearly as permeable as water

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60
Q

how does inner medullary duct absorb urea

A

Inner medullary collecting duct contains specific passive urea transports which facilitates reabsorption
 Only 50% of filtered urea is reabsorbed

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61
Q

Reabsorption – Proximal Tubule % of filtered load of sodium & water reabsorbed. cl as well

A

65%.  Cells of proximal tubule designed for high reabsorption capacity of sodium and water.  Little less percentage for chloride  Quantity can be increased or decreased as needed

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62
Q

Proximal Tubule Cellular Ultrastructure. Contain large number of

A

mitochondria to support extensive active transport activity

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63
Q

Proximal Tubule Cellular Ultrastructure. Luminal (apical) brush border provides

A

huge surface area for rapid diffusion

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64
Q

Proximal Tubule Cellular Ultrastructure. Basolateral border contains

A

extensive number channels in between cells providing huge surface area

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65
Q

Proximal Tubule Cellular Ultrastructure. Luminal border contains _____ and are responsible for?

A

extensive number of protein carrier molecules
 Co-transport of amino acids and glucose
 Counter-transport of hydrogen ions (move a large quantity of hydrogen ions against small hydrogen ion gradient

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66
Q

Proximal Tubule Cellular Ultrastructure. Basolateral border contains

A

extensive amount of N-K ATPase

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67
Q

Early vs. Late Proximal Reabsorption. first half of tubule

A

 Extensive co-transport of sodium with glucose and amino acids
 Sodium reabsorption carries glucose, bicarb, organic ions leaving chloride resulting in increasing [Cl-]
 105 mEq/L increases to 140 mEq/L

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68
Q

Early vs. Late Proximal Reabsorption. second half of tubule

A

 High chloride concentration favors chloride diffusion
 Some movement may occur through specific chloride channels
 Most glucose & amino acids have been reabsorbed – sodium reabsorption drives chloride reabsorption
 Electrochemical gradient

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69
Q

Changes in Solute Concentrations. Total quantity of sodium in tubule changes but concentration does not change because

A

water reabsorption matches sodium reabsorption

Total osmolarity does not change for the same reason. Proximal tubule highly permeable to water

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70
Q

Changes in Solute Concentrations. Glucose & amino acid concentrations

A

decrease due to extensive reabsorption

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71
Q

Changes in Solute Concentrations. creatinine & Urea are

A

concentrated because they are not reabsorbed

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72
Q

Changes in Solute Concentrations. Total amount of Na+, Cl-, HCO3-, glucose, amino acids in tubule

A

decrease

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73
Q

Changes in Solute Concentrations. Total amount of creatinine and urea in tubule

A

does not change

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74
Q

Secretion of Organic Acids & Bases. Many end products of metabolism are secreted by_____ and what are they?

A

proximal tubule.

 Bile salts  Oxalate  Urate  Various catecholamines

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75
Q

Secretion of Organic Acids & Bases. drugs and toxins secreted

A

 Penicillin  Salicylates

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76
Q

Secretion of Organic Acids & Bases. % of para aminohippuric acid

A

90% of PAH in renal blood flow is removed  Can be used to determine renal blood flow

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77
Q

Functional Segments of LOH

A

 Thin descending segment  Thin ascending segment  Thick ascending segment

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78
Q

Thin Descending & Ascending Segment CHARACTERISTICS

A

 Thin epithelial membrane  No brush border  Few mitochondria  Minimal metabolic level

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79
Q

Thin Descending Segment characteristics

A

 Highly permeable to water  Moderately permeable to
most solute
 Allows diffusion of water and solutes
 No active reabsorption  20% of water reabsorption
occurs in the loop of Henle
 Thinascendingsegment impermeable to water
 Part of mechanism for concentrating urine

80
Q

Thick Ascending Segment characteristics

A



Thick epithelial cells with high concentration of mitochondria
 High level of metabolic activity
 Able to reabsorb sodium, chloride, & potassium (Approx 25% of filtered load)
 Also reabsorbs calcium, bicarb, & magnesium
Impermeable to water
 As solute reabsorb luminal solute concentrations drop especially since water NOT reabsorbed – Fluid very dilute

81
Q

Sodium Reabsorption driven by

A

N-K ATPase in basolateral border of tubule cells

82
Q

1 Na-2Cl-1K co-transport mechanism

A

Primary means of moving sodium out of
lumen into tubular cells
 Potassium reabsorbed AGAINST potassium concentration gradient
 Cl- & K+ diffuse out of cell into renal interstitial fluid via specific ion channels

83
Q

other transport mechanism for moving Na from tubular lumen

A

Na-Hcounter-transport mechanism

84
Q

Loop diuretics (furosemide, ethacrynic acid, bumetanide) inhibit the action of _____and equals

A

1Na-2Cl- 1K co-transport mechanism
 Less sodium reabsorption – less water reabsorption in later segments of the nephron
 Less sodium reabsorption – less potassium reabsorption with potential loss of potassium

85
Q

Reabsorption of Other Solutes. Na-Cl-K co-transport mechanism is isoelectric BUT

A

K able to diffuse back into lumen via potassium channels creating +8 mV positive charge in tubule lumen

86
Q

Reabsorption of Other Solutes. Electrical gradient created from k ability to diffuse back into lumen drives diffusion of

A

Na+, K+, Mg++ & Ca++ into the renal interstitial space via the tight junctions (paracellular diffusion)

87
Q

Early Distal Tubule characteristics

A

Macula densa forms first part of tubule
 Part of juxtaglomerular complex
 Provides feedback control for GFR and blood flow (for this nephron)
Next segment high convoluted
 Solute reabsorption – no water reabsorption
 Diluting segment of distal tubule

88
Q

Early Distal Tubule ____% of filtered load for sodium & chloride reabsorbed. and driven by

A

5% Na-K ATPase in basolateral border of tubular cells

89
Q

Early Distal Tubule. Na-Cl co-transport mechanism moves

A

Na+ and Cl- into cell down [Na+]

 Chloride diffuses out of cell via chloride specific channels

90
Q

Early Distal Tubule Thiazide diuretics inhibit

A

this Na- Cl co-transport mechanism. Reduces sodium and chloride reabsorption and ultimately water reabsorption in later segments of nephron

91
Q

Tubular Reabsorption & Secretion

Late Distal Tubule & Cortical Collecting Duct. Sodium reabsorption controlled by

A

various hormones but especially by aldosterone

92
Q

tubular Reabsorption & Secretion

Late Distal Tubule & Cortical Collecting Duct. Potassium secretion controlled by

A

various hormones but especially by aldosterone

93
Q

tubular Reabsorption & Secretion

Late Distal Tubule & Cortical Collecting Duct Able to secrete

A

hydrogen ions against large concentration gradient (1000:1) Proximal tubule moves hydrogen ions against small gradient (4 to 10:1)

94
Q

tubular Reabsorption & Secretion

Late Distal Tubule & Cortical Collecting Duct . Water permeability controlled by

A

oncentration of antidiuretic hormone (ADH, aka vasopressin)
 No ADH - no water permeability – excrete dilute urine
 Increased concentrations of ADH increase permeability of water and decrease the volume of urine and increase the concentration of the urine

95
Q

t.ubular Reabsorption & Secretion

Late Distal Tubule & Cortical Collecting Duct. Membranes impermeable to

A

urea  All urea entering exits to collecting duct to be excreted  Some reabsorption of urea will occur in medullary collecting ducts

96
Q

Late Distal Tubule & Cortical Collecting Tubule types of cells

A

 Principal cells  Intercalated cells

97
Q

principal cells fxn.

A

 Reabsorb sodium &

water  Secrete potassium

98
Q

intercalated cells fxn.

A

 Reabsorb potassium  Secrete hydrogen

99
Q

what drives principal cell activity

A

Na-KATPaseinbasolateral borders of tubule cells drives activity. Sodium follows concentration gradient – diffuses through sodium specific channels
 Potassium follows concentration gradient out of cell into tubular lumen via potassium specific channels

100
Q

Potassium Sparing Diuretics

Aldosterone antagonists

A

Mineralocorticoid receptor antagonists
 Compete with aldosterone receptor sites which inhibits sodium reabsorption & potassium secretion
 Spironolactone & eplerenone

101
Q

Potassium Sparing Diuretics

Sodium Channel Blockers

A

 Inhibit entry of sodium into cell which reduces amount of sodium transported by Na-K ATPase
 Also reduces secretion of potassium as action of Na-K ATPase decreases
 Amiloride & triamterene

102
Q

Intercalated Cell Activity

A

 Secretion controlled by H- ATPase transporter
 Presence of carbonic anhydrase allows conversion of CO2 and H2O to hydrogen ions and bicarb ions
 Chloride also secreted following electrochemical gradient
 Bicarb reabsorbed using Cl- HCO3- counter-transport mechanism following the Cl- gradient into the cell
 CO2 moved freely between cell and interstitial fluid
 Potassium is also reabsorbed

103
Q

Meduallary Collecting Duct Reabsorb less than

A

<10% of filtered water and sodium

104
Q

Meduallary Collecting Duct determine

A

final concentration of solutes and urine concentration

105
Q

Meduallary Collecting Duct water permeability and mitochondria content

A

Epithelial cells smooth with few mitochondria

 Water permeability controlled by ADH

106
Q

urea reabsorption in medullary collecting duct

A

urea is reabsorbed via specific urea transporters which moves urea into the interstitial spaces thus affecting osmolarity

107
Q

hydrogen ions in medullary collecting duct

A

secretes hydrogen ions (like cortical collecting tubule)

108
Q

Change in solute concentration depends on

A

rate of reabsorption (secretion) versus rate of water reabsorption

109
Q

if in item is highly concentrated in the urine that means

A

Items highly concentrated not needed by

body

110
Q

provides indication of water reabsorption

A

Inulin neither secreted or reabsorbed provides indication of water reabsorption

111
Q

 Inulin conc of 3 means that

A

1/3 of water remains in tubule (2/3 has been reabsorbed)

112
Q

Inulin conc of 125 means

A

1/125 of water remains while 124/125 has been reabsorbed

113
Q

Regulation – Tubular Reabsorption ways

A

 Glomerulotubular balance  Peritubular Capillary & interstitial forces  Arterial blood pressure  Hormonal control  Sympathetic nervous effect
 Reabsorption of some solutes can be controlled independently

114
Q

Glomerulotubular Balance Allows an increase in reabsorption rate when

A

there is an increase in tubular load (increased tubular inflow)

115
Q

Glomerulotubular Balance If GFR went from 125 mls/minute to 150 mls/minute rate of reabsorption in proximal tubule would go from

A

81 mls/minute [65% of GFR] to 97.5 mls/minute [65% of GFR]

116
Q

Glomerulotubular Balance works to maintain

A

sodium and volume homeostasis

 Prevents large changes in fluid flow to distal tubules even though there have been significant changes in MAP

117
Q

Peritubular Capillary & Interstitial Forces Relationship of

A

hydrostatic and oncotic pressures AND filtration coefficient

118
Q

peritubular capillary oncotic and hydrostatic pressure

A

32 in 13 out

119
Q

interstitial oncotic and hydrostatic pressure

A

15 out 6 in

120
Q

net absorption / rate peritubular capillaries

A

10 mmHg. 124 mls/ minute 124/10=12.4 mls/min/mmHg

121
Q

increase Peritubular hydrostatic pressure (PHP) [PHP

A

decrease reabsorption

122
Q

increase arterial pressure

A

increase PHP decrease reabsorption

123
Q

esistance of afferent & efferent arteriole increase resistance –

A

decrease PHP increase reabsorption

124
Q

Peritubular oncotic pressure increase POP

A

increase reabsorption

125
Q

increase plasma protein conc.

A

increase plasma oncotic pressure –increases POP increase reabsorption

126
Q

increase GFR or decrease RBF causes

A

an increase in filtration fraction

127
Q

increase filtration fraction

A

increase protein concentration (more fluid is actually filtered) increase POP increase reabsorption

128
Q

Factors Affecting Peritubular Capillary Reabsorption

Renal interstitial hydrostatic and colloid osmotic pressures are affected by

A

changes in reabsorptive forces of peritubular capillaries

129
Q

decrease in capillary reabsorption produces

A

increase in interstitial solute AND interstitial water increase in interstitial hydrostatic pressure AND decrease in interstitial oncotic pressure
decrease in net movement (i.e. reabsorption) of solute & water from renal tubules to renal interstitial spaces

130
Q

Under normal reabsorptive conditions there is always backflow of water & solute from

A

interstitial spaces to tubular lumen (tight junctions not very tight especially in proximal tubule)

131
Q

decrease in peritubular reabsorption causes

A

solute & water accumulation in interstitial space -increase backflow of solute and water from interstitial space into tubular lumen

132
Q

Forces that increase peritubular capillary reabsorption also increase

A

movement of solute and water (reabsorption) from the tubular lumen to the renal interstitial spaces [Reverse also true]

133
Q

increase filtration coefficient

A

increases reabsorption

134
Q

increase surface area

A

increase FC increase reabsorption

135
Q

increase capillary permeabilty

A

increase FC increases reabsorption

136
Q

Filtration Coefficient remains

A

constant under most physiologic conditions. Will be affected by renal disease

137
Q

Even though autoregulation works to keep GFR and RBF constant as pressure changes (75 mmHg to 160 mmHg), there is a small increase in

A

GFR which results in an increase in urine output

138
Q

As arterial pressure increases there is a small decrease in the amount of

A

sodium & water reabsorbed. Small increase in peritubular capillary hydrostatic pressure with subsequent increase in renal interstitial hydrostatic pressure and increase backflow of solute and water

139
Q

As arterial pressure increased angiotensin II release is decreased which means

A

less stimulation of sodium reabsorption by angiotensin Less stimulation of aldosterone production which means less stimulation of sodium reabsorption

140
Q

Hormonal Control

 Kidneys must be able to respond to changes in intake of specific substances without changing

A

output of the substances

141
Q

Hormone secretion provides the control specificity needed

A

to maintain normal body fluid volumes and solute concentrations

142
Q

aldosterone site of action and effects

A

collecting tubule and duct , increase NaCl/H2O reabsorption increase K+ secretion

143
Q

angiotensin 2 site of action and effects

A

Proximal tubule; Thick ascending loop of Henle / distal tubule; Collecting duct
increase NaCl, H2O reabsorption increase K+ secretion

144
Q

ADH site of action and effects

A

Distal tubule; Collecting tubule & duct

increase H2O reabsorption

145
Q

Atrial natriuretic peptide site of action and effects

A

distal tubule; Collecting tubule & duct

decrease NaCl reabsorption

146
Q

parathyroid hormone

A

Proximal tubule; Thick ascending loop of Henle; Distal tubule
decrease PO4— reabsorption increase Ca++ reabsorption

147
Q

Aldosterone Secreted by

A

zona glomerulosa cell in adrenal cortex

148
Q

aldosterone regulates

A

odium reabsorption and potassium secretion

 Very important regulator of [potassium]

149
Q

aldosterone Principal site of action is

A

principal cells of cortical collecting tubule  Stimulates increased Na-K ATPase activity (basolateral locations)  Increases permeability of luminal side membrane to sodium

150
Q

aldosterone Increased release stimulated by:

A

increased extracellular potassium concentration

 Increased angiotensin II levels (i.e. sodium / volume depletion or low arterial pressur

151
Q

aldosterone pathophysiology

A

 Absence (adrenal malfunction or destruction) (Addison’s disease)  Excess(adrenaltumors)(Conn’ssyndrome)

152
Q

Angiotensin 2 most porweful

A

sodium-retaining hormone

153
Q

Angiotensin 2 Increased production caused by

A

low blood pressure and/or low ECF

volume

154
Q

Angiotensin 2 action

A

Stimulates aldosterone secretion (sodium reabsorption) Constricts efferent arterioles (sodium and water reabsorption)
 Helps ensure that normal exertion rates of metabolic wastes are maintained by helping to maintain normal rates of GFR
 Able to retain sodium & water without retaining metabolic waste

155
Q

Angiotensin 2 Direct stimulation of sodium reabsorption in

A

proximal tubules, loop of Henle, distal tubules, and collecting tubules
 Stimulate increased Na-K ATPase activity of tubular epithelial cells (basolateral membrane)
 Stimulate Na-H exchange in proximal tubule (luminal membrane)  Stimulate Na-Bicarb co-transport (basolateral membrane)

156
Q

Angiotensin 2 Affects transport on both

A

uminal and basolateral membranes

 Very active in proximal tubule but also effective in loop of Henle, distal tubule, collecting tubule

157
Q

ADH Made in

A

he hypothalamus
 Two types of magnocellular (large) neurons produce ADH
 Neurons located in supraoptic and paraventricular nuclei  83%insupraoptic  17% in paraventricular nuclei

158
Q

Once produced ADH moves

A

down the neurons to their tips which are located in the posterior pituitary

159
Q

ADH released from

A

neurons in posterior pituitary

160
Q

ADH Stimulation of the supraoptic and paraventricular nuclei (increased osmolarity) sends impulses down the

A

magnocellular neurons which stimulates release of ADH from storage vesicles located in the nerve endings

161
Q

ADH Controls water

A

Permeability of distal tubule, collecting tubule, and collecting duct
decrease [ADH] results in decrease water permeability so water is not reabsorbed which results in increase urine volume and decrease [solute] = large volumes of dilute urine

162
Q

ADH Stimulates formation of ______ by_____

A

water channels across luminal membrane  Binds with specific V2 receptors which increases formation of cyclic
AMP and activation of protein kinases
 Proteinkinaseactivationresultsinmovementofaquaporin-2 (intracellular protein) to luminal side of cell
 Aquaporin-2 molecules come together and fuse with cell membrane to form water channels which increases membrane permeability to water (increase water reabsorption)

163
Q

Chronic increases in ADH will stimulate

A

an increase in formation of aquaporin-2 molecules

164
Q

AVP =

A

arginine vasopressin

165
Q

V2 receptors on

A

basolateral membranes so increase in [ADH] in the plasma will result in movement of ADH from peritubular capillaries to the renal interstitial space

166
Q

Other aquaporins are present on the basolateral membrane providing water channels
No evidence to show that they

A

are affected by ADH

167
Q

decrease [ADH] results in movement of the aquaporin-2 molecules back into the

A

cytoplasm which reduces the number of water channels and water permeability

168
Q

Atrial Natriuretic Peptide

 Secreted by

A

cardiac atrial cells when atria distended by plasma volume expansion

169
Q

Atrial Natriuretic Peptide action

A

Direct inhibition of sodium & water reabsorption
(especially collecting ducts)
 Inhibits renin secretion (thus inhibits angiotensin II formation)

170
Q

Atrial Natriuretic Peptide important response to

A

to help prevent sodium and water retention during heart failure

171
Q

Parathyroid Hormone

 Most important hormone for

A

regulating calcium

172
Q

Parathyroid Hormone action

A

 Increases calcium reabsorption (distal tubules)  Inhibits phosphate reabsorption (proximal tubule)  Increases magnesium reabsorption (loop of Henle)

173
Q

Sympathetic Nervous System

 Severe stimulation results in constriction

A

of renal arterioles which decrease GFR

174
Q

Sympathetic Nervous System low levels of stimulation

A

alpha-receptors on renal tubular epithelial cells (proximal tubule, thick ascending limb of loop of Henle, maybe distal tubule)
Receptor activation stimulates sodium reabsorption which decrease sodium and water excretion

175
Q

Sympathetic Nervous System Stimulates release of renin (angiotensin II) which

A

adds to increase in tubular reabsorption of sodium

176
Q

Renal Clearance def.

A

Volume of plasma that is completely cleared (i.e. all of specified solute) by kidneys per unit time

177
Q

Renal clearance Not realistic as no volume of blood completely cleared BUT PROVIDES:

A

 Way to quantify excretory function of kidneys  Way to quantify renal blood flow  Way to quantify glomerular filtration  Way to quantify tubular reabsorption  Way to quantify tubular secretion

178
Q

renal clearance equals

A

(Us X V)/Ps  Cs is clearance of solute
(mls/minute)
 Us is urine concentration of solute (mg/ml)
 V is urine flow (mls/minute)
 Ps is plasma concentration of solute (mg/ml)

179
Q

Estimation of GFR

If solute freely filtered and neither reabsorbed or secreted, then excretion rate

A

the filtration rate

180
Q

Inulin clearance used as measure of

181
Q

Estimation of GFR Creatinine usually used clinically although

A

small amount is reabsorbed

182
Q

Rough estimate of changes in GFR is to look at

A

changes in creatinine concentration – A four fold increase in creatinine concentration means the GFR is one-fourth normal.

183
Q

GFR x Ps=

A

Us x V=(Us x V)/P=Cs

184
Q

amount of inulin filtered =

A

amount of excreted

185
Q

GFR x P inulin=

A

U inulin x V

186
Q

GFR IN TERMS OF inulin clearance =

A

(U inulin x V)/ P inulin =125 ml/min

187
Q

Estimation of Renal Plasma Flow

 If a substance is completely cleared then

A

clearance rate should equal the renal plasma flow

188
Q

PAH clearance provides reasonable estimation

A

renal plasma flow (90% cleared)

189
Q

Actual renal plasma flow can be calculated by

A

dividing the PAH clearance rate by the PAH extraction rate

 PAH Clearance / 0.9

190
Q

TOTAL BLOOD FLOW can be calculated by

A

taking the calculated plasma flow and dividing by (1-HCT)

191
Q

Filtration Fraction =

192
Q

Absorption=

A

Filtered load – Excretion rate

193
Q

secretion=

A

Excretion rate – Filtered load

194
Q

If equal to inulin clearance

A

Substance only filtered, not reabsorbed, not secreted

195
Q

If less than inulin clearance

A

Substance must be reabsorbed`

196
Q

If greater than inulin clearance

A

Substance must be secreated

Physiology (27 decks)

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