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Physiology- CP > Renin-Angiotensin System > Flashcards

Renin-Angiotensin System Flashcards

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1
Q

What is the renin-angiotensin system?

A
  • Regulates blood pressure and blood volume
  • Effects mediated by angiotensin II (Ang II)
  • Ang II also stimulates aldosterone
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2
Q

What does angiotensin II do?

A
  • Vasoconstrictor of small arteries and arterioles
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3
Q

What does aldosterone do?

A

Volume-expanding hormone

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4
Q

What is angiotensinogen?

A
  • Primary precursor inactive protein (453 amino acids long)
  • Constitutively secreted by liver
  • Amino acid sequence contains sequence for Ang I and II so enzymatically cleaved for desired protein
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5
Q

Which parts of the amino acid sequence are Ang I and II?

A
  • Ang I- first 10 amino acids

- Ang II- first 8 amino acids

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6
Q

What is renin?

A
  • Enzyme secreted by the kidney
  • Secreted by juxta glomerulus apparatus- cells in and around glomerulus
  • Release is primary determinate of RAS activated- regulate part
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7
Q

What stimulates the response of renin?

A
  • Released in response to blood pressure

- Sympathetic activation

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8
Q

What does renin do?

A
  • Cleave angiotensin to make Ang I

- No physiological activity

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9
Q

What is the juxtaglomerular apparatus?

A
  • Afferent arteriole –? filtration –> efferent arteriole

- Cells surrounding afferent arteriole release renin

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10
Q

What does ACE stand for?

A
  • Angiotensin Converting Enzyme
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11
Q

What does ACE do?

A
  • Peptidase
  • Cleaves peptide bonds
  • Converts inactive Ang I to active Ang II by cleaving off 2 amino acids
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12
Q

How is ACE expressed?

A
  • Constitutively expressed
  • Mainly in the endothelium of lung
  • Also found in other tissues
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13
Q

What is bradykinin?

A
  • Vasodilator broken down by ACE

- Causes pain, redness and increase in permeability

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14
Q

How is ACE important clinically?

A
  • ACE inhibitor drugs
  • Promote vasodilation
  • Also promote bradykinin
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15
Q

Describe the mechanism of Ang II

A
  • Vascular smooth muscle (Vasoconstriction)
  • Adrenal cortex (aldosterone release)
  • Sympathetic nerves (increase noradrenaline)
  • Kidney (promoting Na+ retention)
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16
Q

What is the overall effect of Ang II?

A
  • Affects blood pressure and blood volume

- Promotes vasoconstriction and salt and water retention

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17
Q

What breaks down Ang II?

A
  • Amino peptidases

- In blood cells in peripheral tissues

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18
Q

What products result from angiotensin II breakdown?

A
  • Limited activity for some products
  • Ang III (Ang2-8) limited vasoconstriction
  • Ang 1-7 vasodilator acting at MAS receptors
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19
Q

What is the endocrine renin system?

A
  • Circulating renin originates in the kidneys mainly

- Physiological actions all around the body

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20
Q

What is the paracrine renin system (local)?

A
  • All components are present in a tissue
  • E.g. kidneys
  • Heart and blood vessel walls
  • Various parts of the brain
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21
Q

What factors increase renin release?

A
  • Low arterial blood pressure
  • Low blood volume
  • Altered sodium handling
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22
Q

How does low arterial blood pressure increase renin release?

A
  • SNS activation via baroreceptor reflex
  • Internal stretch receptor (juxtaglomerular cells)
  • Trigger release of renin
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23
Q

How does low blood volume increase renin release?

A
  • SNS via low pressure receptors

- Arterial stretch

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24
Q

How does altered sodium handling increase renin release?

Study These Flashcards
A
  • Detected by intrarenal mechanism (macula densa)
25
What factors decrease renin release?
- Negative feedback - Increased arterial pressure- decreased SNS activation - Increased blood volume- increases afferent arteriole stretch - Angiotensin II- negative feedback mechanism
26
How is RAS regulated?
- Renin is the point of regulation - Liver continuously produces angiotensin- not rate limiting - ACE constitutively expressed on lung endothelium - Renin release controlled by BP
27
What are the 2 Ang II receptors?
- AT1 receptors | - AT2 receptors
28
Describe AT1 receptors
- Mitogenic, pro-fibrotic (pathologically importnat), vasoconstriction - Predominant receptor
29
Describe AT2 receptors
- Anti-mitogenic, anti-fibrotic, vasodilatory and decrease BP
30
What are the mediated actions of AT1 receptors?
- Control of blood pressure - Vasoconstriction - Aldosterone release from adrenal cortex- leads to Na+ retention, increased osmolality of plasma
31
Describe how vasoconstriction occurs with AT1 receptor stimulation
- Direct action on vascular smooth muscle - Release of ADH and endothelia - Potentiation of SNS - Blockers of RAS referred to as sympatholytic - Multiple vasoconstrictors released
32
Where are AT1 receptors found and what do they do with noradrenaline?
- Potentiate noradrenaline release - Block reuptake - Increase noradrenaline synthesis
33
What are the other sites of action for Ang II?
- Central control mechanisms in medulla of brain - Catecholamine release from adrenal medulla - Overall effect is increased SNS activity
34
Describe the mechanism of Ang II action on receptor
- Ang II act on nerve ending AT1 - Potentiation of sympathetic system - Noradrenaline - Αlpha receptors on blood vessels - Vasoconstriction
35
Describe the action of aldosterone
- Release regulated by Ang II and also high K+ conc - Promotes water retention - Also drives potassium secretion
36
How does aldosterone promote water retention?
- Osmotic effect of increasing sodium retention in kidney and gut - Increased ADH - Potent dipsogen (promotes thirst)
37
What are the other actions that occur via AT1 receptors?
- Drives a lot of remodelling changes - Mitotic- fibroblasts and smooth muscle - Hypertrophy particularly cardiomyocytes - Profibrotic- inhibits collagen breakdown - These effects are associated with pathological changes in heart failure and chronic kidney disease
38
What are the mediated actions that occur at AT2 receptors?
- Stimulates vasodilation - Increases activity of collagenases- decreasing collagen activity and fibrosis - Decrease growth factor expression and inhibition of tissue growth - Induction of apoptosis
39
How is vasodilation stimulated via AT2 receptors?
- Through NO release | - Increased tissue bradykinin production
40
What is the equation for cardiac output and peripheral resistance?
MAP = CO X TPR
41
How is TPR regulated?
- Regulated by vascular tone - Depends on level of constriction - Small change in radius leads to big change in vasoconstriction
42
What is the relationship between CO and stroke volume?
CO = HR x SV | - Heart rate increased by SNS
43
What is stroke volume determined by?
- Preload- if we expand volume- stretch myocardium and it responds with more force - Contractility - Afterload
44
How does Ang II action affect vasculature?
- Fast-acting short response - Direct vasoconstriction will increase TPR (resistance) - Interaction with SNS and endothelia release
45
How does Ang II action affect blood volume?
- Slower acting, long term - Salt and water retention via direct action and stimulation aldosterone - Increase in venous return (preload) and therefore CO
46
Whats the link between Ang II and heart failure in remodelling?
- Falling BP, baroreceptors constantly not firing, little stimulation, a lot of sympathetic stimulation, a lot of renin - Leads to Ang II release - Profibrotic/mitotic effects- leads to increased cardiac modelling
47
What is the link between Ang II and chronic kidney disease in remodelling?
- Promotes mesangial proliferation and hypertrophy - Promotes synthesis of TGF-β and collagen - Degenerative process elating to glomerulosclerosis
48
List the blockers of RAS
- β-blockers - Renin inhibitors - ACE inhibitors - Angiotensin receptor antagonists
49
How do β-blockers work?
- Block SNS stimulation of secretion
50
How do renin inhibitors work?
- Drugs exist but are not routing clinical use as renin is the only regulator
51
How do ACE inhibitors work?
- Block conversion of Ang I to Ang II
52
How do angiotensin receptor antagonists work?
- Stop Ang II binding to AT1 receptor
53
Describe the mechanism of action of ACE inhibitors
- Block conversion of inactive Ang I to active Ang II - Also inhibits breakdown of bradykinin - Widely used in heart failure - Captopril, ramipril
54
How do ACE inhibitors inhibit the breakdown of bradykinin?
- As a vasodilator, adds to lowering BP - Basis of best known side effect- dry cough - No other benefit
55
How do ACE inhibitors help with heart failure?
- Reduced preload and afterload | - Anti-fibrotic effects
56
When would AT1 receptor antagonists be prescribed?
- Persistent dry cough with ACE inhibitors
57
Give examples of AT1 receptor antagonists
- Losartan | - Candesartan
58
What is the difference between ACE inhibitors and AT1 receptor antagonists?
- Unlike ACE inhibitors, AT1 receptor antagonists do not affect AT2 receptors - Seem equally good in terms of treating heart failure

Physiology- CP (19 decks)

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