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23 spring: pharm > Test 2: lecture 24 RAAS > Flashcards

Test 2: lecture 24 RAAS Flashcards

1
Q

steps of RAAS

A

angiotensinogen (renin) → angiotensin I (ACE) → angiotensin II

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2
Q

ACE is a nonspecific enzyme that cleaves — from diverse substrates like —

A

dipeptides

bradykinin, angiotensin 1

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3
Q

angiotensin III is formed by — and will cause — release

A

angiotensin II (ACE)

aldosterone release

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4
Q

how does angiotensin degraded

A

angioteninases

enzyme breaks angiotensin down in 15-60 seconds

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5
Q

aldosterone will —

A

cause Na and water retention

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6
Q

what does angiotensin do

A

will cause vasoconstriction→ increases BP

causes aldosterone secretion → retension of water and Na from urine

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7
Q

what triggers aldosterone release

A

increased angiotensin II, ACTH, low Na, high K
acidosis
atrial stretch receptors in response to low BP

aldosterone causes retention of Na and water, made by the zona glomerulosa of the adrenal gland

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8
Q

aldosterone is made by —

A

zona glomerulosa cells in the adrenal cortex

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9
Q

effects of RAAS on cardiovascular system

A

vasoconstriction

increased cardiac contractility with little change in heart rate

cause HTN/ fix low BP

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10
Q

effect of RAAS on ANS

A

SYM: causes release of NE and enhances sensitivity of target tissues to NE

Adrenal medulla: causes release of catecholamines from chromaffin cells (↑ epi)

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11
Q

RAAS effect on CNS

A

increase SYM
cause pituitary to release ADH and ACTH
cause increased thirst and need for salty things

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12
Q

effect of RAAS on cell growth

A

cause cardiovascular hypertrophy

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13
Q

overall effect of RAAS on the body

A
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14
Q

AT1 receptors mediate —

A

most of the known functions of angiotensin

will cause smooth muscle contractions in seconds

GPCR receptor

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15
Q

losartan works on what type of receptor

A

angiotensin 1 (AT1) receptor

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16
Q

two major ways to block RAAS

A

ACE inhibitors

angiotensin II receptor blockers (ARBs)

17
Q

benefits of ACE inhibitiors

A

stops formation of angiotensin II

  • decrease systemic vascular resistance without increasing heart rate
  • promote natriuresis (pee out Na)
  • treatment of hypertension, decrease mortality and morbidity in heart failure and left ventricular dysfunction after myocardial infarction
  • delay diabetic nephropathy
18
Q

what are some side effects of ACE-inhibitors

A

will inhibit degradation of other substances (bradykinin and substance P)
cough
angioedema

ACE not specific for only angiotensin

19
Q

captopril

A

ACE inhibitor

will ↓BP and treat CHF

20
Q

what are some ACE inhibitors

A

enalapril, captopril, lisinopril

ACE-I= -pril

21
Q

losartan

A

nonpeptide antagonist of angiotensin 1 (AT1) receptor

does not effect AT2

used to treat HTN

22
Q

what are some ARBs

A

angiotensin receptor blockers/antagonists

peptide congeners: work in theory

nonpeptide antagonist: losartan, Azilsartan (Edarbi), Candesartan (Atacand), Eprosartan

ARBs — sartan

23
Q

angiotensin vs bradykinin

A

angiotensin: works to raise blood pressure

bradykinin acts to lower blood pressure (vasodilation)

24
Q

how to form kinins

A

kiniogens (kinogenases/kallikreins) →kinins

tissue damage and infections activate this class of compounds.

kallikrein-kinin system =KKS

25
Q

where do kallikreins come from

A

made in liver as prekallikreins

cleaved to active kallikrein

kallikrein will bind to kininogens to form kinins

26
Q

where to find kininogens

A

plasma, lymph , intersititial fluid

in plasma: there are a high and low molecular weight versions
high: stays in bloodstream
low: can cross capillary walls into tissues

27
Q

what is the major form of kinins in plasma

A

bradykinin

28
Q

kininase II is the same as

A

ACE

both work on many peptides: kinins and angiotensin

29
Q

which kinin receptor works on bradykinin and kallidin and what does it cause

A

B2 receptor

a BGCR
will cause vasodilation and excretion of Na and pain

30
Q

B2 kinin receptors will bind to — and cause —

A

bradykinin and kallidin

Vasodilation, Na+ excretion, pain

31
Q

B1 kinin receptors binds to — and cause —

A

des-Arg kinins (NOT bradykinin)

Vasoconstriction, pain, leukocyte recruitment

32
Q

what type of receptor has opposite effect as angiotensin 1 receptors

A

bradykinin B2 receptors

B2 cause vasodilation and Na excretion
AT1 cause vasoconstriction and Na retention

33
Q

why are ACE inhibitors cardioprotective

A

ACE inhibitors will block angiotensin II formation and will also prevent the breakdown of bradykinin

ACE inhibitors will decrease BP and work to treat CHF (by getting rid of Na)

23 spring: pharm (46 decks)

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