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3B week 2 - RAAS, electrolytes and acid-bases > RAAS system > Flashcards

RAAS system Flashcards

1
Q

where is renin synthesised stored and released from

A

juxtaglomarular cells (in kidneys) aka renin releasing granular cells

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2
Q

what is the precursor molecule for renin

A

prorenin

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3
Q

what enzymes convert prorenin to renin (2)

A

proteolytic enzymes -> cathepsin B & D

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4
Q

what is the function of renin

A

conversion of angiotensinogen -> angiotenin I

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5
Q

RAAS pathway steps

A

angiotensinogen –(renin)–> angiotensin I –(ACE)–> angiotensin II -> angiotensin III

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6
Q

what increases renin release (4)

A
  1. decreased arterial BP
  2. decreased BP in glomerular vessels (afferent arterioles)
  3. increased loss of Na+ / water (i.e. less Na+ in DCT)
  4. increased sympathetic activity (fight or flight to increase BP)
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6
Q

what is the active form of angiotensinogen

A

angiotensin II

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6
Q

what decreases renin release (3)

A
  1. Na+ / water retention
  2. increased BP
  3. activation of AT1 receptors (short negative feedback loop)
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7
Q

what 3 pathway cotnrol renin secretion

A
  1. macular densa
  2. intrarenal baroreceptor pathway
  3. beta 1-receptor pathway
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8
Q

what is the macular densa pathway of renin control

A
  1. reabsorption of NaCl occurs at the macula densa
  2. increase in NaCl flux causes inhibition of renin release from the juxtaglomerular cells and vice versa
  3. ATP, adenosine and prostaglandins modulate this pathway
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9
Q

what common drug class can affect the macula densa pathway of renin release and why

A

NSAIDs -> inhibit PGE release which reduces renin release via the macula densa pathway

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10
Q

where is the macula densa situated

A

on the thick ascending limb/ distal tubule -> loops round so it is in contact w the afferent and efferent arterioles

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11
Q

what does the juxtaglomerular apparatus consist of (3)

A
  1. macula densa
  2. granular cells
  3. mesangium extra glomerular cells
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12
Q

what channel is responsible for the NaCl absorption by the macula densa

A

Na+/K+/2Cl- symporter

NaCl and K+ into the macula densa cells

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13
Q

what is the channel responsible for the removal of Na+ from the macula densa

A

Na+/K+ ATPase

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14
Q

how is adenosine produced to modulate the juxtaglomerular cell release of renin

A

via the Na+/K+ATPase which results in the byproduction of ADP which is then further broken down into adenosine

i.e. higher NaCl reabsorbtion in to the macula densa = increased adenosine produciton = inhibition of renin for JG cell

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15
Q

what is macula densa regulation usually based on the concentration of

A

[Cl-] -> rather than [Na+] as the [Na+] in the tubular lumen is usually higher than required for saturating the symporter and so changes in Na+ conc usually don’t have an effect as the symporter will remain saturated

16
Q

what is the intrarenal baroreceptor pathway

A
  1. increase in BP or renal perfusion pressure in preglomerular vessles
  2. inhibition of renin release via beta1 receptors on juxtaglomerular cells

i.e. increased BP = descreased renin and vice versa

17
Q

what is the short loop -ve feedback mechanism seen in the RAAS system

A

increase in renin secretion -> increased angiotensin II-> AT1 on JG cells -> decreased renin

18
Q

what factors affect the long loop negative feedback mechanism (3)

A
  1. activation of high pressure baroreceptors
  2. increased renal arterial pressure in the preglomerular vessels
  3. reduced NaCl absoprtion from the proximal tubule
    -> reduction in renin release
19
Q

phsyiological factors modifying renin release (3)

A
  1. systemic BP
  2. dietary salt intake
  3. pharmacological agentsw
20
Q

what drugs can modify renin release

A
  1. NSAIDs -> inhibit PG synthesis
  2. loop diuretics - decrease BP and increased NaCl reabsoption (so less NaCl to stimulate macula densa in the distal tubule) causing increased renin release
  3. ACEi
  4. ARBs
  5. renin inhibitors
  6. BBs -> decrease renin by reducing Beta receptor activation
21
Q

what is angiotensin I converting enzyme

A

a glycoprotein, non-specific enzyme that is identical to kinsae II -> inactivates bradykinin and other potent vasodilators

converts angiotensin I -> angiotensins II

22
Q

when does the RAAS system become ativated

A

decrease in blood volume or blood pressure

23
Q

what kind of receptors are juxtaglomerular cells

A

baroreceptors - detect drop in blood pressure in afferent arterioles

24
Q

where is Na+ resorbed

A
  1. proximal convoluted tubule (65%)
  2. loop of henle (13%)
  3. distal convoluted tubule (5%)
25
Q

why does lower BP result in increased Na+ resorption and what does this mean for renin release

A

blood moves slower through the nephron if BP is lower => there is more time for Na+ to be reabsorbed so more resorption occurs
-> increased renin release as less Na+ detected at macula densa

26
Q

what organ produces angiotensinogen

A

liver

27
Q

what organs produce ACE (2)

A

lungs and kidneys

28
Q

actions of angiotensin II (6) !!

A
  1. systemic vascoconstriction (increases BP)
  2. constricts efferent arterioles (increased GFR, increased Na+ in DCT)
  3. aldosterone release -> results in resorption of Na+ in DCT and excretion of K+(and thus water follows resulting in increased BP)
  4. travels to pit gland and stimulates post. pit to release ADH (water reabsorbed in the collecting duct)
  5. inhibits renin release (increased tubular NaCl resorption which leads to decreased renin release)
  6. increased sympathetica activity
29
Q

what is ACE2

A

an enzyme that acts as a counter balance to ACE -> turns Ang II back into Ang I

30
Q

what is Ang II converted into

A

Angiotensin III (by aminopeptidase A)

31
Q

function of angiotensin III

A

central regulation of hypertension and ADH release

32
Q

where does ADH cause resorption of water from (2)

A
  1. DCT
  2. collecting duct
33
Q

how can Ang I be converted to Ang II without ACE

A

alternate pathway enzymes e.g. cathepsin, tonin, heart chymase

34
Q

what is a rapid pressor response

A

an increase in systolic blood pressure (SBP) of at least 30 mmHg above the baseline or placebo measurements

35
Q

what is the slow pressor response

A

prolonged infusions of angiotensin II (AngII) entails a delayed rise in BP

36
Q

what channel is blocked by furosemide

A

Na+/K+/2Cl- cotransporter in the thick ascending limb of the loop of Hen

37
Q

how does aldosterone affect the cardiovascular systme (6)

A
  1. vascular sm cells hypertrophy and proliferation
  2. increased extracellular matric of vascular sm cells
  3. hypertrophy of cardiac myocytes
  4. increased extracellular matrix production by cardiac myofibroblasts
  5. increased cardiac contractility (opens VG gated Ca2+ channels)
  6. increased cardiac rate (central symapthetic tone)
38
Q

inhibitors of the RAAS system (drug classes - 3)

A
  1. ACEi
  2. ARBs
  3. direct renin inhibitors
39
Q

what layer of the adrenal gland is aldosterone released from

A

glomerulosa

3B week 2 - RAAS, electrolytes and acid-bases (5 decks)

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