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Medical Pharmacology Exam 3 > Renin Angiotensin System, Vasopressin and Kinins > Flashcards

Renin Angiotensin System, Vasopressin and Kinins Flashcards

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USMLE® Step 1 flashcards
1
Q

What are the 3 components of the circumventricular organs?

A

Area postrema
Subfornical organ
Organum vasculosum of the lamina terminalis

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2
Q

Broadly speaking, the MAS receptor is cardio [protective/damaging]. Its ligand is _. The AT2R and AT1R receptors are cardio [protective/damaging], their ligands are _

A

MAS - protective - Ang1-7
AT2R- Damaging - Ang II
AT1R - Damaging - Ang III/ II

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3
Q

Ang I is biologically [active/inactive]. It is converted to Ang II and Ang III by _.

A
  • inactive

- ACE and aminopeptidases

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4
Q

What is the ACE-AngII-AT1 signalling axis known for?

A

Hypertension, stroke and cardiovascular disease

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5
Q

What is the product of ACE2 and endopeptidases? What is the precursor?

A

Ang 1-7

Ang I and Ang II

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6
Q

What is the ACE2-Ang 1-7 -MAS signalling axis known for?

A

Cardioprotective branch of the RAS pathway

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7
Q

What is the source of renin? What is its function?

A

Kidney

Angiotensinogen to angiotensin

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8
Q

What are 3 mechanisms that increase renin release?

A

Decreased afferent arteriole stretch (kidney)
Reduced sodium sensed by macula densa
Increased renal nerve activity

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9
Q

What are 3 molecules that feed back to inhibit renin release?

A

Ang II
Vasopressin (AVP)
Potassium

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10
Q

Feed back inhibition from Ang II is lost when what 2 classes of drugs are used?

A

ACE inhibitors

AT1 receptor blockers

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11
Q

What is the effect of decreased arterial pressure on renin release? What are the two mechanisms enacted?

A

Increased release
Direct mechanism - renal baroreceptors
Indirect mechanism - systemic baroreceptors /baroreflex

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12
Q

What is the effect of dehydration/ hemorrhage on renin release?

A

Increased release

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13
Q

What is the effect of hyponatremia on renin release? What senses this?

A

Increased renin release

The macula densa

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14
Q

What are 4 mechanisms by which Ang II and Ang III raise arterial pressure?

A
  • Direct vasoconstriction (AT1R on smooth muscle)
  • CNS - Increased vasopressin and SNS release
  • Peripheral NS - increased norepinephrine
  • Adrenal medulla - Increased epinephrine release
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15
Q

True or false: Ang II and Ang III are able to cause increase HR and tissue hypotrophy?

A

False, bith cause increased HR and HYPERtrophy

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16
Q

What is the effect of angiotensin on thirst and vasopressin release? What is stimulated to increase thirst?

A

Increases both

Circumventricular organ

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17
Q

What are the effect of angiotensin on the adrenal medulla?

A

Stimulates the release and synthesis of aldosterone

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18
Q

What are the 2 mechanism by which the RAS can be detrimental during heart failure?

A

Increased renin (reduced renal blood flow) leads to

  • increased peripheral resistance (increased afterload)
  • Increased water retention (increased preload)
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19
Q

Which of Ang II, Ang III and Ang 1-7 promotes

  • hypertrophy, tissue remodeling and organ damage
  • counteracts vascular remodeling/hypertrophy and organ damage
A
  • Ang II and Ang IIi first bullet

- Ang 1-7 second bullet (via MAS receptor)

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20
Q

What are 2 mechanism by which the RAS increases sodium retention?

A
  • vasoconstriction (less into glomerulus)

- increased reabsorption from proximal tubule

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21
Q

True or false: Angiotensin receptors are ion channels

A

False, the angiotensin receptors are GPCRs

22
Q

What is the second messenger for AT1R? What is the effect of its activation?

A

Phospholipase C, Calcium and MAPK

Vasoconstriction

23
Q

What is the second messenger of AT2R? What is the effect of its activationb (2)

A

Nitric oxide, also block MAPK

Vasodilation

24
Q

AT1 and AT2 receptors have opposing actions on blood vessels. What are they? Which dominates? Why?

A

AT1 - vasoconstriction
AT2 - vasodilation
AT1 dominates because more of the receptor is present in the blood vessel

25
Q

What is the effect of MAS receptor activation? (3) What are the 2 second messengers?

A

Vasodilation
Antiinflammation
Anti cell proliferation
NO and Calcium

26
Q

What are the 4 examples of AT1 receptor antagonists provided? What condition would they be used for? When would a patient be considered for an AT1 receptor blocker?

A

Losartan, valsartan, candesartan and irbesartan
Heart failure
If a patient doesn’t respond to ACE inhibitors

27
Q

How have the blood pressure lowering effects of AT1 receptor blockers been explained?

A

The residual effects of the AT2 receptor vasodilation and naturesis (no longer counteracted by AT1 mediated vasoconstriction and sodium retention)

28
Q

How can feedback contribute to the blood pressure lowering effects of AT1 receptor blockers?

A

AT1 block = no feedback, increased renin release from kidney, more Angiotensin (and all its metabolites) production, including Ang 1-7 and ACE2

29
Q

What are 3 major side effect of angiotensin receptor blockers?

A

Hypotension
Hyperkalemia
Acute renal failure (in renal insufficiency patients)

30
Q

What are 2 populations where angiotension receptor blockers are contraindicated?

A

Pregnant women

Nursing mothers

31
Q

What are the 6 examples of ACE inhibitors provided?

A 
Captopril
Enalapril
Lisinopril
Ramipril
Quinapril
Fosinopril
32
Q

What are 4 uses of ACE inhibitors?

A

Hypertension (Major use, major agent)
Left ventricular systolic dysfunction
Myocardial infarction
Heart failure

33
Q

In addition to the side effects of AT1 receptor blockers, what are 2 additional side effects of ACE inhibitors? What is the mediating molecule?

A

Dry cough
Angioedema
Bradykinin is mediator of angioedema

34
Q

How may Ang 1-7 play a role in the blood pressure lowering effects of ACE inhibitors?

A

ACE degrades Ang 1-7

ACE also degrades Ang I, a precursor for Ang 1-7

35
Q

What is the example of the renin inhibitor available for the treatment of hypertension? What are its side effects?

A

Aliskiren

Same as ACE inhibs + AT1R inhibs AND GI/allergic symptoms

36
Q

In addition to the kidney, what are 2 additional areas where renin is made?

A

Vascular smooth muscle

Brain

37
Q

What are kinins? What 2 enzyme families make kinins?

A

Vasodialator peptides

Kininogens and kallikreins

38
Q

What is the predominant kinin in the blood? What is its effect on arterioles? Large arteries? Large veins?

A

Bradykinin
Dilates arterioles
Constricts large arteries and most veins

39
Q

What is the effect of kinins infused into normotensive subjects? What is the effect of kinin antagonists in these same subjects? What is the conclusion

A

Vasodilation
No effect in normotensive subjects
- bradykinin is probably important in modulating Pa in hypertensive situations but it does not contribute to maintenance of basal Pa in normotensive subjects

40
Q

What is the effect of kinins on capillary permeability? On the sympathetic ganglia?

A

Increases capillary permeability

Minor - stimulate sympathetic ganglia, also increase epinephrine release

41
Q

In addition to its cardiovascular role, kinins also play a role in what 3 other processes?

A

Glandular secretion
Inflammation (edema)
Pain

42
Q

What type of receptors are the kinin receptor? What is the major physiological agonist? What are the 2 end products of the second messenger system that mediate their effects?

A

GPCRs
Bradykinin
Nitric oxide and prostaglandins

43
Q

The major agonist for the B1 subtype of the kinin receptor is _. It has what effect on vascular smooth muscle?

A

des-Arg-bradykinin

contraction of vascular smooth muscle

44
Q

How does Kininase II link the kinin and angiotensin signalling systems? What drug family inhibits kininase II?

A

Kininase II inactivates bradykinin. It is the same enzyme that converts Ang I to Ang II.
ACE inhibitors

45
Q

What is another name for vasopressin? What is its major function? Mutations in the protein or receptor can lead to what disease?

A

Antidiuretic hormone
Regulation of body osmolality
Diabetes insipidus

46
Q

What are 3 major conditions that can increase the release of vasopressin (ADH)?

A

Decreased arterial pressure
Decreased fluid volume / increased plasma osmolality
pain/nausea/hypoxia/hormones

47
Q

In addition to its antidiuretic actions, what is a direct and an indirect action of vasopressin?

A

Direct - vasoconstriction

Indirect - Bradycardia

48
Q

What are the 2 receptor subtypes for vasopressin? What are their associated g-proteins? What actions do they mediate?

A

V1 - Gq - cardiovascular effects

V2 - Gs - Antidiuretic effects

49
Q

A mutation in which of the vasopressin receptors can cause diabetes insipidus?

A

V2

50
Q

What are the 2 examples of vasopressin antagonists discussed? What is their receptor specificity?

A

Conivaptan - V1/V2

Tolvaptan - V2 selective

51
Q

How do the target diseases for conivaptan and tolvaptan differ?

A

Conivaptan - hyponatremia from SIADH

Tolvaptan - hyponatremia from fluid retention resistant to fluid restriction (CHF, SIADH, cirrhosis)

52
Q

Vasopressin can be pathological in hypertension. It can also be pathological in heart failure. How can antagonists be used to tackle aspects of heart failure mediated by vasopressin?

A

V1 antagonists - reduce afterload

V2 antagonists - treat hyponatremia

Medical Pharmacology Exam 3 (13 decks)

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