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Pharmacology- Test 3 Material > 23- RAS, Vaso, and Kinins > Flashcards

23- RAS, Vaso, and Kinins Flashcards

1
Q

cyclic AMP (cAMP)

A

-activated by AVP activation of V2 receptors

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2
Q

aldosterone

A
  • hormone produced and secreted by adrenal cortex
  • secreted in response to activation of RAS (Ang-II and III) and functions to inc. retention of Na and water to inc. blood pressure
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3
Q

angiotensin

A

-peptides that are formed by combined proteolytic actions of renin and angiotensin converting enzymes [Ang-I, Ang-II, Ang-III, and Ang-(1-7)]

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4
Q

angiotensin converting enzyme (ACE)

A
  • enzyme (ACE1) that converts Ang-I to various active peptides (Ang-II, Ang-III) that have cardioregulatory effects
  • part of classical RAS pathway that can mediate hypertension
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5
Q

ACE2

A
  • enzyme that converts angiotensin I and II to alt. peptide Ang-(1-7) which interacts with Mas receptor
  • this ACE2-Ang-(1-7)-Mas pathway is counterregulatory to classical RAS pathway and has cardioprotective effect
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6
Q

angiotensinogen

A
  • large peptide that is activated by renin secreted from kidneys to form Ang-I
  • initial inactive peptide of RAS pathway
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7
Q

Ang-(1-7)

A
  • created by ACE2 conversion of Ang-I or Ang-II

- interacts with Mas receptor to dec. blood pressure and cause naturesis

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8
Q

AT1 receptor

A
  • predominate receptor of RAS and mediates most actions of Ang-II and Ang-III
  • stimulates phospholipase C (PLC) which inc. intracellular Ca++ and MAPK
  • Ca mediates vasoconstrictive effects
  • MAPK causes cardiac remodeling
  • because AT1 levels > AT2, AT1 effects normally predominate
  • target of ARBs
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9
Q

AT2 receptor

A
  • stimulate inc. in NO release and block MAPK activation
  • mediates vasodilation and natriuresis
  • opposes AT1 mediated vasoconstriction and may be important with AT1 blockade
  • normally AT1 receptor levels > AT2 levels so AT1 effects normally predominate
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10
Q

Mas receptor

A
  • mediates vasodilation, anti-inflammation, anti-cell proliferation opposes AT1 receptor-mediated effects
  • stimulates inc. Ca and NO release
  • activation opposes effects of classical RAS pathway
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11
Q

eicosanoids

A

-release mediated by bradykinin activation of PLA2, which stimulates vasodilation

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12
Q

juxtaglomerular cells (JG cells)

A

-stimulated by SNS to release renin when there is a decrease in blood pressure detected by systemic baroreceptors or inc. renal nerve activity

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13
Q

kininase II

A

-enzyme that creates bradykinin from kininogen/kallikrein

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14
Q

kininogen/kallikrein

A
  • precursors to bradykinin
  • bradykinins are vasodilator peptides
  • broken down by kinase II (ACE1)
  • ACE inhibitors prevent breakdown and cause dry cough
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15
Q

phospholipase A2 (PLA2)

A
  • activated by bradykinin binding to B2 receptor

- causes release of eicosanoids (i.e. prostaglandins) which mediates dilation

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16
Q

phospholipase C (PLC)

A
  • activated by AT1 receptor and causes release of Ca (vasoconstriction) and MAPK (cardiac remodeling)
  • also modulates inc. Ca++ when bradykinin binds to B2 which inc. pain, contraction, and NO
17
Q

renin

A
  • enzyme secreted by the kidneys in response to:
    1. dec. stretch of renal vessels
    2. dec. Na in macula densa
    3. SNS stimulation of juxtaglomerular cells
  • release inhibited by: Ang-II, AVP, high K
  • those on ACEI and ARBs lose feedback inhibition
18
Q

candesartan

A

AT1 antagonist (ARB)

  • primarily used from HTN and heart failure
  • lack some side effects of ACE inhibitors– for patients that don’t tolerate ACE inhibitors
  • higher affinity for AT1 receptors than AT2 receptors
  • Do NOT affect kininase II
  • still allow for AT2 activation and may increase production of Ang-(1-7)
  • blocking AT1 results in loss of AII feedback inhibition of renin release (increased release of renin leading to AI and AII being metabolized to Ang-(1-7) by ACE2)
  • side effects- hypotension, hyperkalemia, acute renal failure in patients with renal insufficiency
  • Contraindicated in pregnant and nursing mothers
19
Q

irbesartan

A

AT1 antagonist (ARB)

  • primarily used from HTN and heart failure
  • lack some side effects of ACE inhibitors– for patients that don’t tolerate ACE inhibitors
  • higher affinity for AT1 receptors than AT2 receptors
  • Do NOT affect kininase II
  • still allow for AT2 activation and may increase production of Ang-(1-7)
  • blocking AT1 results in loss of AII feedback inhibition of renin release (increased release of renin leading to AI and AII being metabolized to Ang-(1-7) by ACE2)
  • side effects- hypotension, hyperkalemia, acute renal failure in patients with renal insufficiency
  • Contraindicated in pregnant and nursing mothers
20
Q

losartan

A

AT1 antagonist (ARB)

  • primarily used from HTN and heart failure
  • lack some side effects of ACE inhibitors– for patients that don’t tolerate ACE inhibitors
  • higher affinity for AT1 receptors than AT2 receptors
  • Do NOT affect kininase II
  • still allow for AT2 activation and may increase production of Ang-(1-7)
  • blocking AT1 results in loss of AII feedback inhibition of renin release (increased release of renin leading to AI and AII being metabolized to Ang-(1-7) by ACE2)
  • side effects- hypotension, hyperkalemia, acute renal failure in patients with renal insufficiency
  • Contraindicated in pregnant and nursing mothers
21
Q

valsartan

A

AT1 antagonist (ARB)

  • primarily used from HTN and heart failure
  • lack some side effects of ACE inhibitors– for patients that don’t tolerate ACE inhibitors
  • higher affinity for AT1 receptors than AT2 receptors
  • Do NOT affect kininase II
  • still allow for AT2 activation and may increase production of Ang-(1-7)
  • blocking AT1 results in loss of AII feedback inhibition of renin release (increased release of renin leading to AI and AII being metabolized to Ang-(1-7) by ACE2)
  • side effects- hypotension, hyperkalemia, acute renal failure in patients with renal insufficiency
  • Contraindicated in pregnant and nursing mothers
22
Q

captopril

A

ACE inhibitor

  • uses: HTN, LV systolic dysfunction, MI, heart failure
  • BP loweing effects may be mediated by increased production of Ang-(1-7)
  • side effects- DRY COUGH, angioedema (d/t bradykinin) hypotension, hyperkalemia, acute renal failure in renal insufficiency
  • Contraindicated in pregnant and nursing mothers
23
Q

enalapril

A

ACE inhibitor

  • uses: HTN, LV systolic dysfunction, MI, heart failure
  • BP loweing effects may be mediated by increased production of Ang-(1-7)
  • side effects- DRY COUGH, angioedema (d/t bradykinin) hypotension, hyperkalemia, acute renal failure in renal insufficiency
  • Contraindicated in pregnant and nursing mothers
24
Q

lisinopril

A

ACE inhibitor

  • uses: HTN, LV systolic dysfunction, MI, heart failure
  • BP loweing effects may be mediated by increased production of Ang-(1-7)
  • side effects- DRY COUGH, angioedema (d/t bradykinin) hypotension, hyperkalemia, acute renal failure in renal insufficiency
  • Contraindicated in pregnant and nursing mothers
25
Q

conivaptan (Vaprisol)

A

Vasopressin receptor antagnoist

  • V1 and V2 receptor antagonist
  • Tx of hyponatremia 2/2 SIADH
  • available as IV drug.
26
Q

tolvaptan (Samsca)

A

Vasopressin receptor antagnoist

  • Selective V2 receptor antagonist.
  • Tx of hypervolemic and euvolemic hyponatremia that is resistant to fluid restriction (ie HF, cirrhosis, SIADH).
  • PO preparation
27
Q

aliskiren (Tekturna)

A

Renin inhibitor

  • used for essential HTN
  • S/E: same as ARB’s and ACEI with addition to GI and allergic Sx.
  • Not as effective for pt with HTN and low renin levels.

Pharmacology- Test 3 Material (10 decks)

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