Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Physiology- CP > Renin-Angiotensin System > Flashcards

Renin-Angiotensin System Flashcards

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What does angiotensin II do?

A
  • Vasoconstrictor of small arteries and arterioles
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What does aldosterone do?

A

Volume-expanding hormone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What stimulates the response of renin?

A
  • Released in response to blood pressure

- Sympathetic activation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What does renin do?

A
  • Cleave angiotensin to make Ang I

- No physiological activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the juxtaglomerular apparatus?

A
  • Afferent arteriole –? filtration –> efferent arteriole

- Cells surrounding afferent arteriole release renin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What does ACE stand for?

A
  • Angiotensin Converting Enzyme
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How is ACE expressed?

A
  • Constitutively expressed
  • Mainly in the endothelium of lung
  • Also found in other tissues
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is bradykinin?

A
  • Vasodilator broken down by ACE

- Causes pain, redness and increase in permeability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How is ACE important clinically?

A
  • ACE inhibitor drugs
  • Promote vasodilation
  • Also promote bradykinin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the overall effect of Ang II?

A
  • Affects blood pressure and blood volume

- Promotes vasoconstriction and salt and water retention

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What breaks down Ang II?

A
  • Amino peptidases

- In blood cells in peripheral tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the endocrine renin system?

A
  • Circulating renin originates in the kidneys mainly

- Physiological actions all around the body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What factors increase renin release?

A
  • Low arterial blood pressure
  • Low blood volume
  • Altered sodium handling
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

How does low blood volume increase renin release?

A
  • SNS via low pressure receptors

- Arterial stretch

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How does altered sodium handling increase renin release?

A
  • Detected by intrarenal mechanism (macula densa)
25
Q

What factors decrease renin release?

A
  • Negative feedback
  • Increased arterial pressure- decreased SNS activation
  • Increased blood volume- increases afferent arteriole stretch
  • Angiotensin II- negative feedback mechanism
26
Q

How is RAS regulated?

A
  • 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
Q

What are the 2 Ang II receptors?

A
  • AT1 receptors

- AT2 receptors

28
Q

Describe AT1 receptors

A
  • Mitogenic, pro-fibrotic (pathologically importnat), vasoconstriction
  • Predominant receptor
29
Q

Describe AT2 receptors

A
  • Anti-mitogenic, anti-fibrotic, vasodilatory and decrease BP
30
Q

What are the mediated actions of AT1 receptors?

A
  • Control of blood pressure
  • Vasoconstriction
  • Aldosterone release from adrenal cortex- leads to Na+ retention, increased osmolality of plasma
31
Q

Describe how vasoconstriction occurs with AT1 receptor stimulation

A
  • 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
Q

Where are AT1 receptors found and what do they do with noradrenaline?

A
  • Potentiate noradrenaline release
  • Block reuptake
  • Increase noradrenaline synthesis
33
Q

What are the other sites of action for Ang II?

A
  • Central control mechanisms in medulla of brain
  • Catecholamine release from adrenal medulla
  • Overall effect is increased SNS activity
34
Q

Describe the mechanism of Ang II action on receptor

A
  • Ang II act on nerve ending AT1
  • Potentiation of sympathetic system
  • Noradrenaline
  • Αlpha receptors on blood vessels
  • Vasoconstriction
35
Q

Describe the action of aldosterone

A
  • Release regulated by Ang II and also high K+ conc
  • Promotes water retention
  • Also drives potassium secretion
36
Q

How does aldosterone promote water retention?

A
  • Osmotic effect of increasing sodium retention in kidney and gut
  • Increased ADH
  • Potent dipsogen (promotes thirst)
37
Q

What are the other actions that occur via AT1 receptors?

A
  • 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
Q

What are the mediated actions that occur at AT2 receptors?

A
  • Stimulates vasodilation
  • Increases activity of collagenases- decreasing collagen activity and fibrosis
  • Decrease growth factor expression and inhibition of tissue growth
  • Induction of apoptosis
39
Q

How is vasodilation stimulated via AT2 receptors?

A
  • Through NO release

- Increased tissue bradykinin production

40
Q

What is the equation for cardiac output and peripheral resistance?

A

MAP = CO X TPR

41
Q

How is TPR regulated?

A
  • Regulated by vascular tone
  • Depends on level of constriction
  • Small change in radius leads to big change in vasoconstriction
42
Q

What is the relationship between CO and stroke volume?

A

CO = HR x SV

- Heart rate increased by SNS

43
Q

What is stroke volume determined by?

A
  • Preload- if we expand volume- stretch myocardium and it responds with more force
  • Contractility
  • Afterload
44
Q

How does Ang II action affect vasculature?

A
  • Fast-acting short response
  • Direct vasoconstriction will increase TPR (resistance)
  • Interaction with SNS and endothelia release
45
Q

How does Ang II action affect blood volume?

A
  • Slower acting, long term
  • Salt and water retention via direct action and stimulation aldosterone
  • Increase in venous return (preload) and therefore CO
46
Q

Whats the link between Ang II and heart failure in remodelling?

A
  • 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
Q

What is the link between Ang II and chronic kidney disease in remodelling?

A
  • Promotes mesangial proliferation and hypertrophy
  • Promotes synthesis of TGF-β and collagen
  • Degenerative process elating to glomerulosclerosis
48
Q

List the blockers of RAS

A
  • β-blockers
  • Renin inhibitors
  • ACE inhibitors
  • Angiotensin receptor antagonists
49
Q

How do β-blockers work?

A
  • Block SNS stimulation of secretion
50
Q

How do renin inhibitors work?

A
  • Drugs exist but are not routing clinical use as renin is the only regulator
51
Q

How do ACE inhibitors work?

A
  • Block conversion of Ang I to Ang II
52
Q

How do angiotensin receptor antagonists work?

A
  • Stop Ang II binding to AT1 receptor
53
Q

Describe the mechanism of action of ACE inhibitors

A
  • Block conversion of inactive Ang I to active Ang II
  • Also inhibits breakdown of bradykinin
  • Widely used in heart failure
  • Captopril, ramipril
54
Q

How do ACE inhibitors inhibit the breakdown of bradykinin?

A
  • As a vasodilator, adds to lowering BP
  • Basis of best known side effect- dry cough
  • No other benefit
55
Q

How do ACE inhibitors help with heart failure?

A
  • Reduced preload and afterload

- Anti-fibrotic effects

56
Q

When would AT1 receptor antagonists be prescribed?

A
  • Persistent dry cough with ACE inhibitors
57
Q

Give examples of AT1 receptor antagonists

A
  • Losartan

- Candesartan

58
Q

What is the difference between ACE inhibitors and AT1 receptor antagonists?

A
  • Unlike ACE inhibitors, AT1 receptor antagonists do not affect AT2 receptors
  • Seem equally good in terms of treating heart failure

Physiology- CP (19 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions