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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
Q

B-adrenergic receptor pathway

A

activation of B1 receptors (by SNS-NE) on juxtaglomerular cells-> increas renin release

26
Q

increase circulating angiotenin II leads to

A

decreased renin release

27
Q

regulation of renin release

A
  1. short- loop negative feedback

2. long-loop negative feedback

28
Q

short-loop negative feedback

A

stimulating angiotensin receptors on juxtaglomerular cells-> decrease renin release

29
Q

long-loop negative feedback

A

increase circulating angiotensin II->incr. BP-> decr. renin

30
Q

AT2 receptors

A

often opposite of AT1

- in vasculature mediate vasodilation

31
Q

AT1 receptors in vasculature

A

vasoconstrictors

promotes SM hypertrophy (chronic effect)

32
Q

AT1 receptors in adrenal cortex

A

stimulation of synthesis & secretion of aldosterone

33
Q

AT1 receptors in adrenal medulla

A

stimulation of epinephrine release

34
Q

AT1 receptors in kidney

A
  • efferent arteriole vasoconstriction
    inhibition of renin release from JG cells
  • increase Na rebsorption in the proximal tubule
35
Q

AT1 receptors in heart

A

stimulation of myocardial hypertrophy & collagen synthesis

36
Q

AT1 receptors in brain

A

increased release of vasopressin (ADH), stimulation of thirst & salt appetite, increased central sympathetic outflow

37
Q

pressor effects of angiotensin I through AT1 receptor

A

> PR (Vasoconstriction), aldosterone (retention of Na & H2O), Na retention, sympathetic tone, hypertrophy in blood vessels & myocardium (chronic effect)

38
Q

angiotenin (1-7) effects

A

vasodilation, increased diuresis, anti-inflammatory

39
Q

ACE inhibitors MOA

A
  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
Q

sensitivity to ACEI is increased in patients with

A

activated RAS (low salt diet, HF)-> profound effects

41
Q

in HTN ACEI

A
  • 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
Q

main therapeutic uses of ACEI

A

HTN, left ventricular systolic dysfunction, acute MI, prevention of CAD events & stroke, chronic renal failure

43
Q

how do ACEI cause hyperkalemia?

A

blocking angiotensin II-> decreased aldosterone which can lead to an increase build up of potassium

44
Q

main ADE of ACEI

A

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
Q

how do ACEI cause cough?

A

accumulation of bradykinin, substance P &/or prostaglandins in lungs.
iron supplement may be beneficial

46
Q

AT1 receptor blockers aka

A

ARBs

-sartan

47
Q

ARB result in

A
  • 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
Q

ACEI vs. ARBs

A
  • 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
Q

main therapeutic uses of ARBs

A

HTN, HF, stroke prophylaxis, diabetic nephropathy

50
Q

Main ADE of ARBs

A
  • comparable w/ placebo
  • hypotension, esp. in salt-depleted individuals
  • less potential for angioedema
  • hyperkalemia
  • teratogenic potential
51
Q

renin inhibitor

A

aliskiren

52
Q

aliskiren is indicated for

A

the treatment of HTN as monotherapy & in combo

53
Q

main ADE of aliskiren (renin inhibitor)

A

similar to placebo

- HA, fatigue, dizziness, diarrhea, nasopharyngitis, epistazis (nosebleed), hyperkalemia, hyperuricemia, teratogenic

Cardio exam 1 (12 decks)

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