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Pharm 3, Test 3 > Antihypertensives- RAAS > Flashcards

Antihypertensives- RAAS Flashcards

1
Q

What is the most important component of short and long term BP regulation?

A

RAAS

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2
Q

What is renin?

A

An enzyme that acts on angiotensinogin to form angiotension I

Renin is the rate limiting step in formulating Ang I and II

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3
Q

What secretes renin?

A

Juxtoglomerular cells

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4
Q

What controls renin secretion? 3 pathways

A

Macula densa pathway
Intrarenal baroreceptor pathway
B-adrenergic pathway

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5
Q

Where is the macula densa?

A

In the thick ascending limb

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6
Q

What does the macula densa do?

A

Senses the na content leaving the loop of henle

Regulates renin release from the JG cells

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7
Q

Explain how increased Na affects the macula densa and JG cells

A

Incresed BP leading to increased Na making it to the macula densa causes it to INHIBIT COX 2, which decreases prostoglandins. PGs are what signal to the neighboring JG cell that they need to release more renin. So, less PGs means less signaling to JG cells, causing less renin secretion

Opposite for HYPOtension

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8
Q

How does the intrarenal baroreceptor pathway work?

A

Increases/decreases in bp in the AFFERENT arteriole inhibit/stimulate renin secretion

Believed to work through changes in wall tension, stretch receptors, modifying PG secretion. Basically same concept as the macula densa pathway, just different initiation

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9
Q

What is the B-adrenergic receptor pathway?

A

Mediate by the release of NE from sympathetic postglanglionic nerve terminals. Beta 1 receptors on JG cells enhance renin secretion

In the pathway, it leads to the same result at the level of the JG cells as the other pathways. B1 receptor is Gs coupled, leading to increased AC, causing increased cAMP, leading to release of renin

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10
Q

What is the short loop negative feedback loop for renin release?

A

Increases in renin secretion enhance the formation of Ang II. Ang II stimulates At-1 I receptors on JG cells, inhibiting renin release

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11
Q

How does Ang II activate the negative feedback loop?

A

Activates AT1 receptors on JG cells, which is a Gq coupled receptor. Causes increased Ca secretion, which inhibits renin release

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12
Q

How does the long loop negative feedback work with renin?

A

Renin enhances Ang II formation, activating the same AT1 receptor involved in the short loop feedback. In addition to the short loop, it also causes increased arterial bp. By doing this, it
causes more Na reabsorption (which inhibits renin release)
Increases pressure in the pre glomerular vessels (Which inhibits renin release)
Inactivation of B1 receptor pathway (Less renin, duh)

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13
Q

Which Ang is most potent?

A

Ang II

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14
Q

Why is Ang I clinically almost irrelevant?

A

It is rapidly converted to Ang II

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15
Q

What does ACE1 do to Ang I?

A

Takes 2 amino acids off Ang I, creating Ang II

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16
Q

How does ACE1 affect bradykinin (potent vasodilator)?

A

Inactivates bradykinin

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17
Q

Where is ACE1 found?

A

High amounts found circulating in plasma, especially in the vascular endothelial cells in the lungs

Fun fact, this is where the “cough” from ACE inhibitors factors in

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18
Q

Where is ACE2 found?

A

Circulating plasma, as well as lungs. Same as ACE 1

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19
Q

What is the preferred substrate for ACE2?

A

Ang II

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20
Q

What does ACE2 do to ANG II?

A

Creates Ang (1-7)

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21
Q

Where is angiotensinogen created? Little bit? or a lot?

A

Liver, produced in dump truck loads lol

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22
Q

What converts angiotensinogen to Ang I (1-10)?

A

Renin

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23
Q

What is Ang1(1-10) rapidly converted to? By what?

A

AngII (1-8)

By Ace-1

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24
Q

Which Ang is responsible for the major effects of the RAAS?

A

Ang II

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25
Q

Which Ang is entirely opposite of the others?

A

Ang (1-7)

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26
Q

How is Ang (1-7) formed?

A

Ang II getting cleaved by ACE2 mainly

27
Q

What does Ang (1-7) do?

A

Vasodilator and naturetic effect

28
Q

Where is most AT2 receptors distributed?

A

Fetal tissues

29
Q

What doe activation of AT1 receptors, leading to enhancement of MAPK cause?

A

Increased cellular growth/proliferation

30
Q

How does the rapid pressor response work in the RAS?

A

Ang II is 40x more potent than NE, and it acts rapidly, raising BP in seconds.
This is through AT1 activation

31
Q

How does RAS work as a long term pressor?

A

Persistant release of Ang II leads to a decrease in renal excretory function
increased release of aldosterone
Reduced NaCl excretion
Increased K secretion

32
Q

Why is Ang II vasoconstrictive properties less in some areas?

A

Fight or flight concept. Vasoconstriction in the brain and liver and skeletal muscles is less because it needs increased blood flow

33
Q

What can Ang II stimulate a small amount of release of____

A

NE

34
Q

What is Ang II direct effect on Na in the renal system?

A

Direct Na reabsorption by stimulating the Na/H exchanger in the proximal tubule, increasing Na and Cl and Bicarbonate reabsorption

35
Q

How does Ang II affect renal hemodynamics?

A

Reduced renal blood flow by directly constricting the renal vasculature, enhancing sympathetic tone. and facilitates renal noradernergic neurotransmission

36
Q

Over time, how does the RAS affect the cardio vasculature structure?

A

Increased wall to lumen ration in blood vessels, concentric cardiac hypertrophy (basically thicker walls and thinner lumen), Eccentric hypertrophy (thin wall and large lumen), thickened blood vessel wall

37
Q

What is the MOA of ACE inhibitors?

A

Inhibits conversion of ANG I to Ang II
Causes interference with short and long term feedbacks on renin release
Increases renin release, as well as Ang I
Ang I goes down other routes, forming Ang (1-7)

38
Q

What is Ace inhibitors other effects?

A

Increase bradykinin levels and bradykinin subsequently increases prostaglandin synthesis

39
Q

How does ace inhibitors affect all aspects of bp?

A

Decreases SVR, BP
Blood flow in kidneys increases due to vasodilation
Blood flow in brain remains unchanged

40
Q

How does ace inhibitors affect vascular compliance of large vessels?

A

They increase the compliance, causing there to not be a significant sympathetic outflow of catecholamines. The baroreceptors are less responsive due to the compliance, which is why there isn’t a response by the SNS

41
Q

How does ACE inhibitors affect aldosterone secretion?

A

Lowered in most patients

42
Q

Why is ACE inhibitors helpful in HF?

A

It reduces bp, reducing afterload ultimately, leading to increased CO

43
Q

How do ACE inhibitors affect HR compared to most other antihypertensive drugs?

A

It reduces it (increases compliance and reduces catecholamine release, causing decreased HR)

44
Q

How do ACE inhibitors affect renovascular resistance? Causing what?

A

Decreases and renal blood flow increases, leading to improves natiuresis (elimination of Na) and reduced aldosterone secretion

45
Q

How do ACE inhibitors affect morbidity and mortality in HF pts? Or even in CVD disease?

A

Improves it

46
Q

Can pregnant people take ACE inhibitors?

A

Nope

47
Q

How do Ace inhibitors affect fibrinolytic balance?

A

Reduces plasma levels of plasminogen, promoting fibrinolysis in pts with artery disease

48
Q

How are ACE inhibitors good for renal failure patients?

A

Improves renal vascular blood flow

49
Q

What does “prilat” indicate in ACE inhibitors?

A

They are formulated in a ester prodrug to improve oral absorption

50
Q

What is a obvious ADE in every hypertensive drug?

A

Hypotension. Duh

51
Q

What is important to be aware of with the first few doses of ACE inhibitors?

A

Steep drop in bp

52
Q

What percentage of patients suffer from a cough r/t ACE inhibitors?

A

5-20%

53
Q

How does ACE inhibitors possibly cause ARF? Cuz it is supposed to be helpful in chronic renal failure…

A

Because initial doses can lead to renal vasculature dilation (Due to blockage of Angiotensin II), causing decreased perfusion to nephrons

This was the sprinkler analogy

54
Q

What are the main therapeutic uses of ACE inhibitors?

A 
Htn
CHF
MI
CVD reduction
Diabetic nephropathy
55
Q

What are the ARB MOA?

A

Competitively binds to the AT1 receptor (which is what Ang II binds to, which increases everything like BP)

Insurmountable antagonism-The maximal response to Ang II cannot be restored in the presence of the ARB regardless of the concentration of Ang II

56
Q

Are ARBs more selective for AT1 or AT2 receptors?

A

AT1

57
Q

What are the exact things that ARBS ultimately do?

A

Reduces bp, reduces aldosterone secretion, blocks catecholamine release, reduces sympathetic tone, reduces CV structural abnormalities

58
Q

Whats the main difference between ARBs and ACE inhibitors?

A

Nothing really, just slightly different MOA’s

ARBs are better at reducing AT1 receptors
ARBs indirectly activate AT2 receptors

59
Q

How are ARBs distributed?

A

Highly protein bound, but it doesn’t effect much

60
Q

What is Losartans active metabolite?

A

EXP 3174, very potent

61
Q

What are the ADEs of ARBS?

A

Basically the same as ACE inhibitors, minus the cough

So acute renal failure, hyperkalemia, hypotension, teratogenic

62
Q

What is the listed direct renin inhibitor?

A

Aliskiren

63
Q

Whats the problem with Aliskiren?

A

Significant ADE’s
BBW-increases risk of stroke, renal problems, and others
Significant blood pressure drop

Pharm 3, Test 3 (5 decks)

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