Renin-angiotensin System Flashcards

1
Q

Physiology of RAAS

A
  • regulation of BP
  • regulation of plasma volume
  • modulation of sympathetic nervous system
  • stimulation of thirst
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2
Q

Where is renin formed and stored?

A

JG cells

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3
Q

What is the primary regulator of formation and maintenance of Ang II?

A

Renin

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4
Q

Is Ang I active or inactive?

A

Inactive

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5
Q

Is Ang II active or inactive?

A

Active

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6
Q

What does ACE do?

A
  • convert Ang I to Ang II

- breakdown bradykinin to inactive metabolites

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7
Q

Bradykinin can cause what?

A
  • vasodilation (cough, angioedema)

- decrease MAP

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8
Q

Ang II AT1 causes what?

A
  • vasoconstriction (increased TPR, Increased MAP)

- aldosterone release (Na and water retention, increased MAP)

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9
Q

Level of Ang II is dependent on what?

A

Amount of circulating renin and angiotensinogen

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10
Q

Angiotensinogen is formed and secreted continuously by what?

A

Liver

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11
Q

Synthesis of angiotensinogen is increased by what?

A

Insulin
Estrogens
Glucocorticoids

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12
Q

Renin is secreted from ____ in response to changes in ____

A

Kidney

BP/volume

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13
Q

What is the clinical test for renin activity? What is the relationship with dietary Na?

A

PRA

Inverse relationship with dietary Na intake

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14
Q

Renin secretion is regulated by (3)

A
  1. Blood volume/pressure (baroreceptors)
  2. Na Cl flux across macula
  3. Sympathetic nervous system activity
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15
Q

Baroreceptors and renin

A

Decreased bp/volume —> decreased stretch —> increased renin

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16
Q

The macula densa is sensitive to what changes?

A

NaCl reabsorption

17
Q

Macula densa and renin

A

Decrease NaCl reabsorption —> increase renin

18
Q

Stimulation of what receptors on JG cells cause renin release

19
Q

SNS activity and renin

A

Increase SNS activity —> increase renin release

20
Q

What are the 2 negative feedback loops of renin?

A
  1. Ang II stimulation of AT1 receptors on JG cells (short)

2. Ang II induced increases in BP (long)

21
Q

How is Ang I formed?

A

Angiotensinogen —> Ang I

**renin RLS

22
Q

Where is ACE found?

A

On endothelial cell surface

23
Q

What is the major active component of RAS?

24
Q

Ang II and K

A

Increase excretion of K

25
Ang II and afferent arteriole
Constrict —> decrease glom pressure —> decrease GFR
26
Ang II and efferent arteriole
Constrict —> increase glomerular pressure —> increase GFR
27
Normal conditions of Ang II and GFR
Afferent constricts slightly more than efferent | **no change or slight decrease GFR
28
Renal arterial hypotension and Ang II
Afferent is maximally dilated | GFR maintained by Ang II mediated constriction fo efferent
29
T/f you can 100% inhibit ACE
False! | There are alternative pathways for ang II synthesis that do not involve renin or ACE
30
How does Ang II alter cardiovascular structure?
AT1 receptor activation
31
Ang II VT1 activation
- stimulate migration, proliferation and hypertrophy of VSM cells - increased production of extracellular matrix - hypertrophy of cardiac myocytes
32
2 major subtypes of Ang II
AT1 (Gq) | AT2 (Gi)
33
Which receptors mediate most biological effects of Ang II?
AT1
34
Where are Ang II AT1 receptors found?
VSM
35
Where are AngII AT2 receptors found?
Fetal tissue
36
What receptor are poorly defined and may exert antiproliferative, proapoptotic, vasodilatory and antihypertensive effects?
AT2
37
What is the prototype ACEI?
Captopril