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Mandies Pharm III > RAS, vasopressin, and kinins > Flashcards

RAS, vasopressin, and kinins Flashcards

1
Q

Angiotensin II interacts with _____ receptors and angiotensin III interacts with ______ receptor

A

AT1/2

AT1

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2
Q

which receptor produces HTN, stroke, CV events

A

ACE-AII-AT1

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3
Q

Mas receptor p’way

A

alternative processing of AI and AII by ACE2 or endopeptidases leads to to the alt peptide Ang 1-7
Mas comprises a counterregulatory, cardioprotective branch of the classical RAS p’way

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4
Q

where is ACE1 present

A

endothelial vascular cells, luminal side

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5
Q

where is renin released

A

in kidney, by juxtoglomerular apparatus

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6
Q

4 mechanisms that control renin release

A
  1. renal vascular receptors in the afferent arteriole (stretch)
  2. macula densa receptor (increased release w decreased Na)
  3. SNS. increased renal nerve activity leads to norepi release leads to beta adrenoreceptors on JG leads to increased renin
  4. AII, vasopressin, K all inhibit release of renin.
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7
Q

why do pt on ACE inhibitors have high renin/AI levels

A

no fb inhibition from AII. (ACE2 is insensitive to ACE inhibitors)

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8
Q

what stimulates renin release

A
  1. decreased arterial pressure (via renal baroreceptors and systemic baroreceptors)
  2. dehydration/hemorrhage (barorecptors in atrium, ventricle, and pulm veins response to decreased BV; chemoreceptors in hypothalamus also respond)
  3. hyponatremia (sensed by macula densa)
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9
Q

how does angiotensin raise BP (4 actions)

A
  1. direct vasoconstriction via AT1 receptors presens on smooth muscle (increase Ca) & slow pressor effect independent of this action
  2. in CNS, increase SNS activity and vasopressin release
  3. in PNS, stimulation of norepi release from symp neurons
  4. adrenal medulla: stim release of epi
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10
Q

other CV effects of angiotensin

A
  1. increases HR and contractility, but often offset by the baroreflex
  2. hypertrophy/tissue remodeling by both non hemodynamic and hemodynamic mechanisms. nonhemodynamic mechanisms involve direct actions of these peptides on vascular smooth muscle cell growth
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11
Q

central actions of angiotensin

A
  • stimulates drinking and increases secretion of ACTH and vasopressin (more angio II than III, much more potent)
  • ACTH stimulates synthesis/release of aldosterone (actions of AII/AIII equal here)
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12
Q

renal actions of angiotensin

A

promotes sodium retention by vasoconstriction and increasing prox tubular Na reabsorption, regulates own production by inhibition to renin release

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13
Q

AT1 receptor

A

G-pro coupled receptor, most actions of AII, AIII are believed to be mediated by this receptor
-stimulates phospholipase C to increase Ca, causes constriction and increases MAPK (proliferative responses, like hypertrophy and tissue remodeling)

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14
Q

AT2 receptor

A
  • does not activate phospholipase C or Ca signaling, but stimulates increases in NO and blocks MAPK activation.
  • vasodilation and natriuresis
  • opposes AT1 -medicated vasoconstriction and may be important in effects of AT1 receptor blockers. AT1 > AT2 in blood vessels.
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15
Q

Mas

A

mediates vasodilation, anti-inflammation, anti-cell proliferation opposes AT1 receptor mediated effects. increases Ca/NO

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16
Q

losartan

A

ARB (AT1 receptor blocker)

  • primarily used for HTN, HF
  • potent non-peptide competitive antagonist of AT1 receptors w high specificity
  • lack some SE of ACE inhibitors, considered for patients that don’t tolerate ACE inhibitors
  • higher affinity for AT1 than 2 or Mas
  • don’t affect kininase II (enzyme that degrades bradykinin, identical to ACE)
  • BP lowering may be medicated in part by residual AT2 receptor activation
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17
Q

valsartan

A

ARB (AT1 receptor blocker)

  • primarily used for HTN, HF
  • potent non-peptide competitive antagonist of AT1 receptors w high specificity
  • lack some SE of ACE inhibitors, considered for patients that don’t tolerate ACE inhibitors
  • higher affinity for AT1 than 2 or Mas
  • don’t affect kininase II (enzyme that degrades bradykinin, identical to ACE)
  • BP lowering may be medicated in part by residual AT2 receptor activation
18
Q

candesartan

A

ARB (AT1 receptor blocker)

  • primarily used for HTN, HF
  • potent non-peptide competitive antagonist of AT1 receptors w high specificity
  • lack some SE of ACE inhibitors, considered for patients that don’t tolerate ACE inhibitors
  • higher affinity for AT1 than 2 or Mas
  • don’t affect kininase II (enzyme that degrades bradykinin, identical to ACE)
  • BP lowering may be medicated in part by residual AT2 receptor activation
19
Q

irbesartan

A

ARB (AT1 receptor blocker)

  • primarily used for HTN, HF
  • potent non-peptide competitive antagonist of AT1 receptors w high specificity
  • lack some SE of ACE inhibitors, considered for patients that don’t tolerate ACE inhibitors
  • higher affinity for AT1 than 2 or Mas
  • don’t affect kininase II (enzyme that degrades bradykinin, identical to ACE)
  • BP lowering may be medicated in part by residual AT2 receptor activation
20
Q

role of Ang-(1-7) in ARB use

A

-BP lowering effects of ARBs may be mediated in part via increased prod of Ang-(1-7)

21
Q

SE of ARBs

A

-hypotension, hyperkalemia, ARF (esp in patients w renal insufficiency, AII/AIII maintain GFR). contraindicated in pregnant/nursing mothers

22
Q

captopril

A

ACE inhibitors
uses: antihypertensive (esp essential HTN), LV systolic dysfuntion (reduces mortality), MI (reduces mort), HF (reduces mort)

23
Q

enalapril

A

ACE inhibitors
uses: antihypertensive (esp essential HTN), LV systolic dysfuntion (reduces mortality), MI (reduces mort), HF (reduces mort)

24
Q

lisinopril

A

ACE inhibitors
uses: antihypertensive (esp essential HTN), LV systolic dysfuntion (reduces mortality), MI (reduces mort), HF (reduces mort)

25
Q

adverse effects of ACE inhibitors

A

captopril, enalapril, lisinopril

-same as ARBs: hypotension, hyperkalemia, ARF, plus dry cough and agioedema due to bradykinin

26
Q

role of Ang-(1-7) in ACEI actions

A

-bp lowering effects of ACEIs may be mediated in part via increased production of Ang-(1-7), this is a result of loss of ACE mediated degredation of Ang-(1-7). Also loss of conversion of Ai to AII would 1. lead to more AI for synthesis of Ang-(1-7) and more release of renin which would generate more AI

27
Q

aliskiren

A

non-peptide based renin inhibitor that is approved for rx of essential HTN
-same SE of ARBs and ACEI plus GI/allergic symptoms

28
Q

effect of RAS blockade in normotensive pt

A

no effect, unless Na depleted

29
Q

is the effect of RAS blockade dependent on high renin in HTN patients

A

no

-also works w renal disease/obstruction HTN

30
Q

local RAS vascular smooth muscle

A

provides local intrinsic control

31
Q

local RAS in brain

A

function as neurotransmitter, regulation of SNS, ADH release, regulation of arterial pressure and metabolism

32
Q

plasma kallikrein vs tissue kallikrein

A

plasma kallikrein activates HMW, bloodstream kininogen to bradykinin; tissue kallikreins convert LMW kininogen to kallidin, which can convert to bradykinin

33
Q

bradykinin

CV effects

A

t1/2 15 sec, acts where formed, autocoid causing vasodilation

  • predominant kinin in blood
  • potent vasodilator of arteriorles via NO and eicosanoids which lower BP
  • increase capillary permeability
  • directly stimulate sympathetic ganglia
  • stimulate EPI release
34
Q

what activates kallikreins

A

viruses, inflammation, cell death

35
Q

in normotensive persons, role of bradykinin

A

-important in modulating Pa in hypertensive situations but it does not contribute to maintenance of basal Pa in normotensive agents

36
Q

bradykinins on large arteries and veins

A

constriction

37
Q

bradykinin other effects

A
  • glandular secretion [salivary glands, pancreas functional vasodilation for secretion]
  • inflammation (edema, increased BF, elevated kinin in various inflammatory situations)
  • pain, stim sensory neurons, releases neuropeptides
38
Q

kinin receptors

A

all G pro coupled receptors
b2 agonists (not beta)
bradykinin and kallidin are equally effective
-mediates majority of effects of BK
-activates PLC, which increases Ca and leads to pain, contraction, NO
-activates PLA2 leads to eicosanoids (prostaglandins)
vasodilation is mediated by NO and prostaglandin production

39
Q

B2 antagonists

A

-are being developed for rx pain, asthma, chronic inflammatory diseases
(bradycor)
-others: peptide and nonpeptide

40
Q

B1 receptor

A
  • prefers a diff form of bradykinin (des-Arg bradykinin)

- mediates contraction of vascular smooth muscle

Mandies Pharm III (10 decks)

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