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Pharmacology Exam 4 > Renin-angiotensin System > Flashcards

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

A

B1

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?

A

Ang II

24
Q

Ang II and K

A

Increase excretion of K

25
Q

Ang II and afferent arteriole

A

Constrict —> decrease glom pressure —> decrease GFR

26
Q

Ang II and efferent arteriole

A

Constrict —> increase glomerular pressure —> increase GFR

27
Q

Normal conditions of Ang II and GFR

A

Afferent constricts slightly more than efferent

**no change or slight decrease GFR

28
Q

Renal arterial hypotension and Ang II

A

Afferent is maximally dilated

GFR maintained by Ang II mediated constriction fo efferent

29
Q

T/f you can 100% inhibit ACE

A

False!

There are alternative pathways for ang II synthesis that do not involve renin or ACE

30
Q

How does Ang II alter cardiovascular structure?

A

AT1 receptor activation

31
Q

Ang II VT1 activation

A
  • stimulate migration, proliferation and hypertrophy of VSM cells
  • increased production of extracellular matrix
  • hypertrophy of cardiac myocytes
32
Q

2 major subtypes of Ang II

A

AT1 (Gq)

AT2 (Gi)

33
Q

Which receptors mediate most biological effects of Ang II?

A

AT1

34
Q

Where are Ang II AT1 receptors found?

A

VSM

35
Q

Where are AngII AT2 receptors found?

A

Fetal tissue

36
Q

What receptor are poorly defined and may exert antiproliferative, proapoptotic, vasodilatory and antihypertensive effects?

A

AT2

37
Q

What is the prototype ACEI?

A

Captopril

Pharmacology Exam 4 (7 decks)

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