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Cardio exam 1 > RAAS lecture > Flashcards

RAAS lecture Flashcards

1
Q

Renin-angiotensin system is an important regulator of

A

blood pressure (short & long term) & hydromineral balance

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2
Q

how many groups of drugs target RAS?

A

3- at different levels

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3
Q

protein

A

a macromolecule with large amino acid sequence (>50 AAs)

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4
Q

peptide

A

a short amino acid sequence (20-30 AAs)

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5
Q

proteolytic enzyme/ protease/ peptidase

A

an enzyme that cleaves peptide bonds in peptides & proteins

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6
Q

receptors

A

proteins (usually located on the plasma membrane) to which ligands (hormones, NTs) bind & cause certain effects

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7
Q

what enzyme converts angiotensinogen to angiotensin I?

A

renin

-rate liming step**

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8
Q

is angiotensinogen active or inactive?

A

inactive

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9
Q

is angiotensin I active or inactive?

A

inactive

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10
Q

angiotensinogen

A

us a glycoprotein synthesized & secreted by liver

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11
Q

renin

A

an enzyme (protease) synthesized, stores & released into circulation by juxtaglomerular cells of kidney

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12
Q

angiotensin I

A

is an inactive peptide, precursor of active angiotensin- formed in systemic circulation

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13
Q

what cells produce renin

A

juxtaglomerular cell

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14
Q

what enzyme converts angiotensin I to angiotensin II?

A

ACE

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15
Q

angiotensin converting enzyme (ACE)

A

protease on the membrane of vascular endothelial cells & circulating in blood
- also degrades bradykinin

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16
Q

angiotensin II

A

main active peptide, formed in systemic circulation, acts through AT1 & AT2 receptors

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17
Q

AT1 receptors is the mediator of

A

pressor effects

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18
Q

angiotensin (1-7)

A

some effects are opposite of angiotensin II; mediated through its own receptor (Maz receptor)
- can be formed from both angiotensin I &II

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19
Q

what enzyme converts angiotensin I to angiotensin (1-7)?

A

NEP (neutral endopeptidase)

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20
Q

what enzyme converts angiotensin II to angiotensin (1-7)?

A

ACE2

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21
Q

increase release of renin leads to

A

more angiotensin II & ELEVATED BP!

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22
Q

what are the 3 long-loop pathways that regulate renin release?

A
  1. macula densa pathway
  2. intrarenal baroreceptor pathway
  3. B-adrenergic receptor pathway
23
Q

macula densa pathway

A

decrease NaCl flux across macula densa-> increase renin release

24
Q

inrarenal baroreceptor pathway

A

decrease BP in afferent arteriole_> increase renin release

25
B-adrenergic receptor pathway
activation of B1 receptors (by SNS-NE) on juxtaglomerular cells-> increas renin release
26
increase circulating angiotenin II leads to
decreased renin release
27
regulation of renin release
1. short- loop negative feedback | 2. long-loop negative feedback
28
short-loop negative feedback
stimulating angiotensin receptors on juxtaglomerular cells-> decrease renin release
29
long-loop negative feedback
increase circulating angiotensin II->incr. BP-> decr. renin
30
AT2 receptors
often opposite of AT1 | - in vasculature mediate vasodilation
31
AT1 receptors in vasculature
vasoconstrictors | promotes SM hypertrophy (chronic effect)
32
AT1 receptors in adrenal cortex
stimulation of synthesis & secretion of aldosterone
33
AT1 receptors in adrenal medulla
stimulation of epinephrine release
34
AT1 receptors in kidney
- efferent arteriole vasoconstriction inhibition of renin release from JG cells - increase Na rebsorption in the proximal tubule
35
AT1 receptors in heart
stimulation of myocardial hypertrophy & collagen synthesis
36
AT1 receptors in brain
increased release of vasopressin (ADH), stimulation of thirst & salt appetite, increased central sympathetic outflow
37
pressor effects of angiotensin I through AT1 receptor
> PR (Vasoconstriction), aldosterone (retention of Na & H2O), Na retention, sympathetic tone, hypertrophy in blood vessels & myocardium (chronic effect)
38
angiotenin (1-7) effects
vasodilation, increased diuresis, anti-inflammatory
39
ACE inhibitors MOA
1. decr, formation of angiotensin II 2. incr. cicrulating bradykinin 3. incr. formation of antiotensin (1-7) (indirectly) also increase renin levels bc of the negative feedback loop is not functional
40
sensitivity to ACEI is increased in patients with
activated RAS (low salt diet, HF)-> profound effects
41
in HTN ACEI
- decr. vascular resistance & BP - incr. compliance of larger arteries - . slight decrease in GFR - aldosterone secretion is slightly decreased (risk for hyperkalemia) - cardiac function is usually UNCHANGED
42
main therapeutic uses of ACEI
HTN, left ventricular systolic dysfunction, acute MI, prevention of CAD events & stroke, chronic renal failure
43
how do ACEI cause hyperkalemia?
blocking angiotensin II-> decreased aldosterone which can lead to an increase build up of potassium
44
main ADE of ACEI
hypotension, cough, hyperkalemia, acute renal failure(in predisposed pts), modest elevation of SCr, in combo w/ NSAIDs-> decr. GFR, teratogenic effect, rash, angioedema, dysgeusia(loss of taste), neutropenia
45
how do ACEI cause cough?
accumulation of bradykinin, substance P &/or prostaglandins in lungs. iron supplement may be beneficial
46
AT1 receptor blockers aka
ARBs | -sartan
47
ARB result in
- arterial vasodilation & reduction of PR - reduction of serum aldosterone levels inhibition of peripheral sympathetic activity - improvement of hemodynamic profile in heart & kidney - also cause incr. renin (loop feedback in inhibited & incr. angiotensin II in plasma (but binding is prevented)
48
ACEI vs. ARBs
- ARBs reduce activation of AT1 receptors more efficiently - ACEI increase renin but NOT angiotensin II while ARBs increase both - in case of ARBs generated angiotensin II can act on AT2 recptors (often opposite effect of AT1 receptors) - ACEI may increase angiotensin (1-7) more than ARBs - ACEI increase levels of bradykinin
49
main therapeutic uses of ARBs
HTN, HF, stroke prophylaxis, diabetic nephropathy
50
Main ADE of ARBs
- comparable w/ placebo - hypotension, esp. in salt-depleted individuals - less potential for angioedema - hyperkalemia - teratogenic potential
51
renin inhibitor
aliskiren
52
aliskiren is indicated for
the treatment of HTN as monotherapy & in combo
53
main ADE of aliskiren (renin inhibitor)
similar to placebo | - HA, fatigue, dizziness, diarrhea, nasopharyngitis, epistazis (nosebleed), hyperkalemia, hyperuricemia, teratogenic

Cardio exam 1 (12 decks)

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