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z:Physl 210A/B > Renal Lec 6 > Flashcards

Renal Lec 6 Flashcards

1
Q

ADH/ vasopressin (type of hormone)

A

-peptide hormone (fast-acting)

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2
Q

osmoreceptors in …sense

A

hypothalamus sense increases in plasma osmolarity

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3
Q

ADH/vasopressin is produced by

A

cells of the SON of the hypothalamus

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4
Q

SON is in the

A

hypothalamus

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5
Q

SON stands for

A

supraoptic nucleus

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6
Q

vasopressin is stored in the

A

posterior pituitary gland

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7
Q

ADH secreted from

A

posterior pituitary gland

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8
Q

site of ADH action

A

collecting duct cells in kidney

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9
Q

mechanism of vasopressin action

A

alters water permeability of the luminal membrane of collecting duct cells

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10
Q

aquaporins (def.)

A

water channels found in renal tubule cells and other cells

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11
Q

number of aquaporins types in body

A

more than 10

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12
Q

type of aquaporins in proximal convoluted tubule

A

AQP1

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13
Q

type of aquaporins in collecting ducts

A

AQP2, AQP3, AQP4

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14
Q

ADH affects … insertion on… via

A

AQP2 insertion on the luminal side via regulation of AQP2 gene transcription

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15
Q

AQP on basolateral membrane

A

are not regulated by ADH (AQP3/4)

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16
Q

vasopressin receptors are on the (side of membrane)

A

basolateral membrane of tubule

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17
Q

vasopressin action mechanism (after attaching to receptors)

A

-vasopressin receptor activates adenylate cyclase which converts ATP to cAMP which activates PKA and causes a cycle of protein phosphorylation which control insertion of AQP2 in luminal membrane

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18
Q

in absence of ADH

A
  • collecting ducts cells are almost impermeable to water

- extreme loss of large fluid volume (water diuresis)

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19
Q

ADH increased (pee less) by

A

shock, pain, warm, hot weather and water deprivation

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20
Q

ADH decreased (pee more) by

A

cold, humid environment, alcohol

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21
Q

diabetes insipidus

A

pathological condition: water diuresis, produce a large amount of dilute urine

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22
Q

central diabetes insipidus

A

failure to release ADH from posterior pituitary

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23
Q

nephrogenic diabetes insipidus

A

impaired renal tubule (especially in collecting ducts)

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24
Q

water diuresis (+pathological condition)

A
  • only excess water is excreted without excess solute in urine
  • diabetes insipidus
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25
Q

osmotic diuresis (+pathological condition)

A
  • excess solute in urine is always associated with high levels of water excretion
  • uncontrolled diabetes mellitus
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26
Q

relationship between body fluid volume & [Na+] regulation

A

-water reabsorption is dependent on Na+ reabsorption

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27
Q

plasma osmolarity mainly determined by

A

measuring the plasma Na+ concentration

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28
Q

changes in total body [Na+] cause changes in

A

blood volume and blood pressure `

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29
Q

low [Na+] in plasma- short term regulation

A

baroreceptors regulate GFR

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30
Q

low [Na+] in plasma- long term regulation

A

aldosterone promotes Na+ reabsorption (renin. angiotensin II needed for secretion)

31
Q

high [Na+] in plasma- regulation

A

-atrial natriuretic peptide (ANP) regulates GFR and inhibits Na+ reabsorption and aldosterone

32
Q

baroreceptors are (def.)

A

nerve endings that are sensitive to stretch

33
Q

baroreceptors are located in

A
  • carotid sinus
  • aortic arch
  • major veins
  • intrarenal (JG cells of JGA)
34
Q

baroreceptors sense

A

-changes in blood volume, peripheral resistance

35
Q

baroreceptors (decrease in b.p causes)

A

-decrease in stretch, decrease in nerve impulse frequency, activation of (SYM branch) of the ANS, constriction of afferent arteriole, ↓GFR, ↓Na+ filtered , ↓Na+ exerted, ↑ Na+ in plasma

36
Q

aldosterone (def.)

A

steroid hormone secreted from the adrenal cortex

37
Q

aldosterone secretion triggered by

A

low sodium concentration

38
Q

aldosterone effect is

A

long term

39
Q

aldosterone (site of action)

A

-late distal tubule and cortical collecting duct

40
Q

actions of aldosterone

A
  • induces synthesis of Na+ transport protein
  • stimulates Na+ reabsorption
  • reduces Na+ excretion
41
Q

Na+ reabsorption is linked to … secretion

A

K+

42
Q

Na+ reabsorption (mechanism)

A
  • Na+ diffuses into the CCD cell (luminal side), actively transported out of the cell via Na+/K+ ATPase (basolateral)
  • K+ moves actively transported into the cell via Na+/K+ ATPase (basolateral) and diffuses into lumen via potassium channel
43
Q

aldosterone affects which channels?

A
  • Na+ channel on luminal side

- Na+/K+ ATPase on basolateral side

44
Q

aldosterone regulation Na+ level

A
  • low NaCL
  • increased renin secretion
  • increased plasma renin concentration
  • increased plasma angiotensin I concentration
  • increased plasma angiotensin II concentration
  • increased aldosterone release
  • increased aldosterone conc
  • increased Na+ transporter synthesis/activity in CCD
  • increased Na+ reabsorption
45
Q

angiotensinogen secreted by

A

liver

46
Q

renin produced by

A

juxtaglomerular cells of JGA in the kidney

47
Q

renin is (def.)

A

an enzyme that helps control blood pressure

48
Q

ACE stands for

A

Angiotensin-converting enzyme

49
Q

ACE convertes

A

angiotension I to angiotension II

50
Q

angiotensin cause

A

vasoconstriction and raise blood pressure

51
Q

renin-angiotensin system (mechanism)

A

angiotensinogen –> (renin) angiotensin I –> (ACE) angiotensin II–> aldosterone (from adrenal cortex)

52
Q

juxtaglomerular cells (location)

A

-on the wall of the afferent arteriole

53
Q

juxtaglomerular cells are (type of receptors)

A

mechanoreceptors

54
Q

juxtaglomerular cells sense

A

circulating plasma volume

55
Q

low volume associated with

A

low sodium concentration

56
Q

macula densa (location)

A

on wall the the distal convoluted tubule

57
Q

macula densa are (type of receptors)

A

chemoreceptors

58
Q

macula densa sense

A

NaCl load of the filtrate

59
Q

renin conc. in plasma determined by

A

JG cells

  1. sympatheitc input from external barocrecptros
  2. intrarenal baroreceptors (JG cells)
  3. signals from macula densa
60
Q

decreased stretch (low circulating volume)

A

renin release

61
Q

increased stretch (high circulating volume) inhibits

A

renin release

62
Q

renin angiotensin mechanism initiated in response to

A
  • sympathetic stimulation of renal nerves
  • decrease in filtrate osmolarity
  • decreased blood pressure
63
Q

the most important trigger for the release of aldosterone is

A

renin-angiotensin mechanism

64
Q

what stimulates ANP secretion?

A
  • increased NA+ concentration
  • increased blood volume
  • atrial distension (most important)
65
Q

ANP is synthesized and secreted by

A

cardiac atria

66
Q

site of ANP action

A

nephron (several tubular segments)

67
Q

ANP action

A
  • inhibits aldosterone actions
  • inhibits Na+ reabsorption
  • increases GFR and Na+ excretion
68
Q

increase in cardiac atria distension leads to

A

↑ ANP secretion leads to =(all directly or via aldosterone)
-↓ plasma aldosterone, ↓ Na+reabsorption
-afferent dilation, efferent constriction = ↑ GFR
= ↑ Na+ excretion

69
Q

K+ (renal handling)

A
  • most filtered K+ is reabsorbed in proximal tubule + loop of henle
70
Q

collecting duct can secrete

A

a small amount of K+

71
Q

[K+] in urine is regulated in

A

CCD

72
Q

hyperkalemia

A

excess K+ in blood

73
Q

↑ extracellular {K+]

A

stimulation of aldosterone production

↑ [K+] excreted in urine

74
Q

↓ extracellular {K+]

A

no aldosterone produced

↓ [K+] excreted in urine

z:Physl 210A/B (28 decks)

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