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Owenpharm Block 2 > ARB, ACE-I & Renin-I Pharmacology > Flashcards

ARB, ACE-I & Renin-I Pharmacology Flashcards

1
Q

Angiotensinogen is converted to what substance by what enzyme?

A

It is converted to Angiotensin 1 by Renin

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2
Q

Where is Renin produced?

A

Kidneys

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3
Q

Agiontensin 1 is converted to Angiotensin 2 by what enzyme?

A

Angiotensin Converting Enzyme

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4
Q

Angiotensin 2 has what effects?

A

Vasoconstriction, Aldosterone secretion, Sympathetic activation

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5
Q

What cells in the kidney contain Renin?

A

Juxtaglomerular Apparatus

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6
Q

Where does Renin cleave Angiotensin?

A

Between Leucines on C end of peptide

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7
Q

Where does ACE cleave Angiotensin 1 to make Angiotensin 2?

A

Between the Phe and His on the C side of the peptide

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8
Q

What does the macula densa sense as plasma passes?

A

NaCl concentration of plasma

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9
Q

Renin is activated in what larger physiologic condition?

This is sensed by what portion of the kidney?

A

Low sodium conditions

Macula Densa

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10
Q

What other portions of the Kidney can cause Renin release?

A

Intrarenal Baroreceptor in Pre-glomerular vessels

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11
Q

Activation of what adrenergic receptors cause increased Renin release?

A

B1 Adrenergic receptors on Juxtaglomerular cells

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12
Q

What is the mechanism to recognize enough Renin has been released?

A

AT1 receptor on Juxtaglomerular cell activated by Angiotensin 2

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13
Q

What receptor mediates the majority of response from Angiotensin 2?

A

AT1

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14
Q

What effects does activation of AT1 receptor have? (5 items)

A 
Vasoconstriction
Vascular proliferation
Aldosterone secretion
Cardiac myocyte proliferation
Increased sympathetic tone
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15
Q

What effects does activation of AT2 receptor have? (3 items)

A

Vasodilation
Antiproliferation
Apoptosis

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16
Q

What is the second messenger process of the AT1 receptor?

A

AT1 activation (G-protein coupled) –> PIP2 –> IP3 + DAG –> IP3 activates Ca2+ & DAG activates PKC

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17
Q

Where is the AT1 receptor located in the Adrenergic synapse? What effect does it have?

A

The AT1 receptor is pre-synaptic & post-synaptic. Its activation by ANG2 results in increased release of NE which activates postsynaptic alpha1 receptors. ANG2 also activates post-synaptic AT1 receptors which have a director vasoconstrictor effect.

18
Q

What is Aldosterone’s effect on the kidney?

A

Reabsorption of Na and Water in intercalated cells of collecting duct

19
Q

What are the broad effects of RAAS Inhibitors? (4 items)

A

Blood pressure lowering related to plasma renin activity
Decrease blood pressure with no change in heart rate
Can cause hypotension
Can cause fetal wasting in pregnancy

20
Q

RAAS inhibition can occur in three locations in the RAAS pathway. What are they?

A

Direct inhibition of Renin release
Inhibition of ACE conversion from Ang1 to Ang2
Blockade of Angiotensin receptor

21
Q

What is the hallmark AT1 receptor blocker medication?

A

Losartan

22
Q

What type of inhibition does Losartan produce on AT1 receptors? What ramifications does this have?

A

Competitive inhibition

Increased Angiotensin 2 production can overcome the Losartan inhibition of AT1

23
Q

What is the mechanism of action of Losartan?

What effects does this produce? (3 items)

A

Angiotensin 2 receptor (AT1) competitive inhibition

  1. Decreased aldosterone secretion
  2. Decreased vasoconstriction
  3. Decreased sympathetic activation
24
Q

Does Losartan and other ARBs work immediately? If not, how long do they take to create maximal effect?

A

No, 4 weeks

25
Q

What adjunct medication is frequently used to increase BP lowering effect?

A

Diuretics

26
Q

What are the hallmark ACE inhibitors for this course? (3 items)

A

Captopril
Enalapril
Lisinopril

27
Q

ACE inhibitors prevent production of what substance from what substance?

A

They prevent production of Ang2 from Ang1

28
Q

What diagnostic would you check to decide if and ARB or ACE-inhibitor is indicated instead of another HTN medication?

A

Draw plasma Angiotensin 2 levels to check for inappropriate elevation.

29
Q

How do black individuals’ response to ACE-I and HCTZ compared to non-black individuals?

A

The percentage of blacks who are responders to ACE-I is significantly less while the percentage who respond to an HCTZ type diuretic was slightly increased. Percentage for combination was about the same.

30
Q

What is the effect of ACE-I on CHF mortality?

A

40% reduction after 6 months

31
Q

What effect did ACE-I (Captopril) have after acute MI? (2 items)

A

Reduction in mortality AND Reduction in LV dysfunction

32
Q

How do ACE-I compare with other vasodilator therapy in CHF therapy?

A

Overall reduction in mortality

33
Q

What is the most common adverse effect of ACE-I?

A

Cough

34
Q

What are the #2-5 common adverse effects of ACE-I? (4 items)

A
  1. Rash
  2. Taste Disturbance
  3. Angioedema
  4. Proteinuria
35
Q

Why would an ACE-I exacerbate renal dysfunction/failure?

A

If the failure is a result of poor perfusion from the Renal artery, ACE-I will prevent compensation to improve perfusion.

36
Q

What is the hallmark Renin inhibitor for this course?

A

Aliskiren

37
Q

What is the mechanism of action of Aliskiren?

A

Aliskiren occupies the binding site for Angiotensinogen on Renin preventing conversion/production of Angiotensin 1.

38
Q

Does Aliskiren increase/decrease/not change systolic, diastolic and HR?

A

Decreases both systolic and diastolic

Doesn’t change HR

39
Q

On what cells in the kidney are Spironolactone and Eplerenone active?

A

Principal cells and Intercalated cells

40
Q

What effect does Spironolactone and Eplerenone have?

A

Inhibition of the renal and extra renal actions of aldosterone (including Na and Water retention)

Owenpharm Block 2 (11 decks)

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