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CVPR > CVPR Week 8: RAAS > Flashcards

CVPR Week 8: RAAS Flashcards

1
Q

Objectives

A
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2
Q

The conversion of angiotensinogen into angiotensin I

A
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3
Q

How large is the angiotensinogen protein?

A

57 kDa

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4
Q

What happens in the conversion of angiotensinogen to angiotensin I?

A

14 amino acids in amino-terminal are cleaved by renin

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5
Q

Where is angiotensinogen produced?

A

It is synthesized by the liver

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6
Q

What determines the rate of angiotensin I formation?

A

concentration is important

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7
Q

What increases the concentration of angiotensinogen?

4 listed

A
  • Corticosteroids
  • Estrogens
  • Thyroid hormone
  • Pregnancy
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8
Q

Identify

A
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9
Q

Identify

A
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10
Q

Where is Renin produced?

A

synthesized by the granular juxtaglomerular cells of the kidney

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11
Q

What releases Renin?

A

Granular Juxtaglomerular cells

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12
Q

What controls the release of Renin?

A

Macula densa cells in the distal tubule control the release of Renin

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13
Q

Factors that control active Renin release from granular juxtaglomerular cells

5 listed

A
  • Macula densa mediators
  • β1-adrenergic receptor activation by NE or Epi
  • granular juxtaglomerular cell stretch
  • Angiotensin II negative feedback effect:
  • ANP-BNP
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14
Q

Macula densa mediators of renin release

A
  • decreased Na+ = increased PGE2 release = increased cAMP = increased Renin
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15
Q

β1-adrenergic receptor activation mediators of renin release

A

increased cAMP = increased renin

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16
Q

Granule juxtaglomerular cell stretch control of renin release

A
  • mediated by increased Ca2+ permeable stretch receptor
  • decreased stretch (vasodilation through α1 block, vasodilators, diuretics, anesthetics) = increased renin
  • Increased stretch (vasoconstriction through α1 receptor activation, angiotensin II = decreased renin
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17
Q

Angiotensin II negative feedback effect control of renin release

A

angiotensin II receptor - increased [Ca2+] = decreased renin

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18
Q

ANP-BNP control of renin release

A

increased cGMP = decreased renin

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19
Q

Describe the conversion of angiotensin I to angiotensin II

A
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20
Q

ACE AKA

A

Angiotensin-converting enzyme

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21
Q

ACE functions

A
  • converts angiotensin I to angiotensin II
  • breaks down bradykinin
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22
Q

Effects of angiotensin II

A
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23
Q

Angiotensin II potency in vasoconstriction

A

40 times more potent than norepinephrine

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24
Q

Angiotensin II vasoconstriction mechanism

A
  • Direct effect via angiotensin II receptor activation of Gq and PLC increasing IP3 levels and release of Ca2+ from intracellular stores.
  • Rho kinase is also activated decreasing myosin light chain phosphatase activity
  • Angiotensin II can also increase peripheral resistance via effects on the CNS by increasing sympathetic tone
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25
Angiotensin II reflex bradycardia
there is little to no bradycardia because angiotensin II rests the baroreceptor reflex
26
Angiotensin II effect on the renal circulation
constricts the efferent glomerular arteriole maintaining glomerular filtration rate
27
Effects of angiotensin II
28
Drug classes that inhibit the renin-angiotensin-aldosterone system 5 listed
* Renin release blockers * Renin inhibitors * ACE inhibitors * Angiotensin II receptor blockers * Aldosterone antagonists
29
Renin release blockers 2 listed
* β-blockers * centrally acting α2 agonists
30
Renin inhibitors
Aliskiren
31
ACE inhibitors
Captopril
32
Angiotensin II receptor blockers
Losartan
33
Aldosterone antagonists
* spironolactone * eplerenone
34
β-blockers and RAAS
counteract the harmful effects of sympathetic and RAAS over-activation
35
β-blockers uses and mechanisms of improving outcomes
They are particularly useful in heart failure, cardiomyopathy and coronary artery disease * decrease remodeling * improve survival * decreased incidence of sudden death/arrhythmias * use in stable heart failure patients without substantial fluid retention
36
Prototype β-blocker
Metoprolol
37
38
Metoprolol clinical uses
* heart failure * cardiomyopathy * coronary diseases
39
β-blockers side effects
* bronchospasm * bradycardia * heart block * heart failure (uncompensated patients) * sedation * sleep disturbances * depression * impotence * mask hypoglycemia * dyslipidemia * rebound hypertension * aggravate peripheral vascular disease
40
Renin inhibitor prototype
Aliskiren
41
Aliskiren uses
hypertension
42
Aliskiren side effects
* teratogen * increased creatinine * hyperkalemia * hypotension
43
Aliskiren interactions
* prevents increases in plasma renin activity caused by other agents, including diuretics, Ca2+ channel blockers and vasodilators * renal impairment, hyperkalemia, hypotension in combination with ARBs or ACEIs * renal impairment with NSAID diuretics
44
ACE inhibitors mechanism
45
Mechanisms of cardiac benefits of ACE inhibitors
* Hemodynamic actions (i.e. vasodilation and decrease in intravascular volume) * decrease in remodeling
46
Indications for ACE inhibitors
* Heart failure * hypertension monotherapy * hypertension associated with CHF or diabetes * Cardioprotective after acute myocardial infarction * Delay the progression of kidney disease, including diabetic nephropathy
47
ACE inhibitors adverse effects and mechanisms
* Cough * Angioedema * Teratogen * Increased creatinine * Hyperkalemia * Hypotension
48
ACE inhibitors and renal vascular autoregulation
49
ACE inhibitors drug interactions
* K+ sparing diuretics, K+ supplements and K+ iodide = risk of hyperkalemia * Increase effects of other anti-hypertensive meds (e.g. hypovolemic patients taking diuretics, also be careful with patients on NaCL restricted diets or with GI disorders)
50
ACE inhibitors prototype
Captopril
51
Captopril uses
* heart failure * hypertension * chronic kidney disease * diabetic nephropathy
52
Captopril side effects
* cough * angioedema * teratogen * increased creatinine * hyperkalemia * hypotension
53
Angiotensin II receptor blockers prototype
Losartan
54
Angiotensin II receptor antagonist mechanism
55
Angiotensin II receptor antagonist in heart failure
56
Losartan uses
* heart failure * hypertension * chronic kidney disease * diabetic nephropathy
57
Losartan side effects
* Angioedema (less common) * teratogen * increased creatinine * hyperkalemia * hypotension
58
Losartan interactions
* K+ sparing diuretics, K+ supplements and K+ iodide = risk of hyperkalemia * Increase effects of other anti-hypertensive meds (e.g. hypovolemic patients taking diuretics, also be careful with patients on NaCL restricted diets or with GI disorders)
59
Aldosterone antagonists mechanism of action
60
Aldosterone antagonists prototypes
* Spironolactone * Eplerenone
61
Aldosterone antagonists clinical uses
62
Aldosterone antagonists toxicity
63
Spironolactone and gynecomastia
64
Overview
65

CVPR (93 decks)

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