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Pharm > Vasoactive drugs shuffled > Flashcards

Vasoactive drugs shuffled Flashcards

1
Q

What’s an important vasoactive peptide that decreases BP?

How does it do so?

Short or long T1/2?

A

Atrial natriuretic peptide (ANP)

Diuretic, vasorelaxant

Short T1/2

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2
Q

Besides using NO donors, how else could impotence be treated?

A

Sildenfal (Viargra)

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3
Q

Which NO donor has an “ultrashort” duration of action (how long is this)?

A

Inhaled amyl nitrate

(3-5 minutes)

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4
Q

Name 5 important classes of vasoactive peptides in the body.

A
  1. Angiotensins (I, II and III)
  2. Bradykinin and related kinins
  3. Vasopressin
  4. Atrial natriuretic peptides and related peptides
  5. Endothelins
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5
Q

______________ may be useful in impotence.

A

NO donors

Nitroglycerine ointment and nitroglycerine patches have been used.

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6
Q

Bosentin: MoA?

A

Endothelin receptor inhibitor

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7
Q

How is NO related to reperfusion?

A

lNO has been shown to protect against ischemic and reperfusion injury.

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8
Q

Pancreatic kallikrein can be activated by ___________.

A

trypsin

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9
Q

Describe the physiologic process that can generate endogenous nitric oxide.

A

*Generated from the oxidation of the guanidine group of arginine (L-arginine –> L-citrulline)

(Exposure to bacterial LPS result in the generation of NO in the macrophage.)

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10
Q

What are the actions of angiotensin II?

What dz can result if it’s overproduced?

A
  • Exerts profound effects in the regulation of vascular tone, fluid and electrolyte balance.
  • It stimulates aldosterone production from the adrenal cortex.
  • At higher concentrations it produces glucocorticoid biosynthesis

HTN & disorders of hemodynamics

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11
Q

Name (or read) some areas where prekallikreins are found. Where are they produced?

A

Kallikreins are glycoprotein enzymes produced in the liver as prekallikreins and are present in:

  • plasma
  • kidney
  • pancreas
  • gastrointestinal tract
  • sweat glands
  • salivary glands
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12
Q

Do the angiotensin antagonists have any effect on the actions on ACE?

A

No, only block receptor

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13
Q

What anti-inflammatory drug also has an effect on molecules generated by bradykinin? (explain, simply)

A

Aspirin is also known to block the algesic effects of prostaglandins generated by bradykinin.

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14
Q

What agents are useful during organ transplantation to preven accelerated graft atherosclerosis?

A

Nitric oxide acts as a cytoprotective agent and prevents cellular and platelet adhesion.

Dietary arginine supplements are helpful in the management of transplantation patients

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15
Q

What does angiotensinase do?

A

Inactivates ANG II and ANG III

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16
Q

What size of a peptide is ANG II?

ANG I?

A

*Octapeptide

Decapeptide

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17
Q

Desmopressin (DDAVP): MoA?

A

Vasopressin analogue

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18
Q

Desmopressin: indications?

A

Bleeding (restore factor VIII and vWF); control bleeding in minor surgeries.

(initially created for diabetes insipidus–vasopressin deficiency)

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19
Q

Explain in detail how NO affects platelets.

A

NO is a potent inhibitor of platelet adhesion, activation, aggregation, & regulates the release of 5-HT, growth factors, and TXA from platelets.

Platelets contain constitutive and inducible NOS’s

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20
Q

Kinins represent one of the most potent groups of vasodilators peptides produced by the endogenous actions of enzymes known as ___________ or ___________.

A

kallikreins or kininogenases

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21
Q

Bosentin: route of administration?

A

PO

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22
Q

Pharmacologically, kinins stimulate the release of what 3 compounds?

Kinins promote water and solution passage from the blood to extracellular fluid resulting in __________.

A

NO, PGE2, and PGI2.

edema

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23
Q

How is the coagulation cascade related to kallikrein?

A

Factor XII (Hageman’s factor) catalyzes the formation of kallikrein, which can go on to make bradykinin from HMW kininogen

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24
Q

Which NOS isoform is a/w chronic/acute inflammation?

A

NOS-3 (endothelial)

Recall: NO promotes edema + vascular permeability.

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25
Q

How does atherosclerosis affect NO?

What vascular effects does this lead to?

A

Impairs NO formation

results in vascular defects and increased cellular proliferation

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26
Q

Besides vasodilation, what other symptoms do kinins produce?

A

Kinins promote redness, local heat, swelling and pain (algesic).

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27
Q

What receptor subtypes can endothelins (ETs) bind?

A

ETA and ETB

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28
Q

What is the indication for ACE inhibitors? (captopril, enalapril)

A

HTN

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29
Q

Bradykinin is released by _________ kallikrein

A

plasma (not sure if important)

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30
Q

How big of a peptide is bradykinin?

What condition is it’s overproduction a/w?

A

Nonapeptide

Hypotensive shock

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31
Q

How many isoforms of angiotensin are there? Which is the most active form (we care about)?

A

Angiotensin II

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32
Q

Name the (3) drugs that are known as “vasopeptide inhibitors”

What enzyme do they inhibit?

What are their physiological actions?

A

Omipatrilat, sampartilat, fasidotrilat

Inhibit MMPs

Enhance vasodilation, reduce vasoconstriction and increase sodium excretion

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33
Q

Name all of the NO inhibitors in this lecture.

A

N-monomethyl-L-arginine (N-MMLA)

N-nitro-L-arginine methyl ester (N-NAME)

7-nitroindazole

BBS-2

Hemoglobin

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34
Q

Compare and contrast the beneficial and toxic effects of nitric oxide.

A
  • The beneficial effects include smooth muscle relaxation, vasodilation, immune regulation, anesthetic and anti-athlerosclerotic responses.
  • The pathologic responses include free radical formation, nitrosation and irritant effects.
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35
Q

What cels possess NOS-2?

A

Inducible iNOS

  • Macrophages, smooth m. cells
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36
Q

What are the indications are angiotensin receptor inhibitors? (losartin, valsartin)

A

HTN

37
Q

_____________ and _____________ are useful in the treatment of atherosclerotic disorders.

A

L-arginine and nitric oxide donors

38
Q

What enzymes can synthesize NO?

Identify the isoforms of the enzymes responsible for the synthesis of nitric oxide.

A

Nitic oxide synthase

  1. NOS-1, neuronal NOS, or nNOS
  2. NOS-2, inducible NOS, or iNOS
  3. NOS-3, endothelial NOS, or eNOS
39
Q

Vasopeptide inhibitors inhibit what type of enzyme?

Thus, these drugs increase the levels of _________________ and decrease the formation of _________________.

A

Metalloproteases

natriuretic peptides, angiotensin II

40
Q

Excess production of NO results in the generation of ______________, which is toxic to cells. Thus, NO inhibitors may be helpful in the treatment of sepsis related disorders.

A

Peroxynitrite

41
Q

Name 4 inhibitors of NO.

A
  1. L-arginine Derivatives (L-NMMA, L-NAME)
  2. Inhibitors of nitric oxide synthase synthesis
  3. Inhibitor of binding of arginine to NOs
  4. Scavengers of NO
42
Q

Which of the NOS isoforms have a calcium requirement?

A

NOS-1 (neuronal) and NOS-3 (endothelial) only

43
Q

How many types of bradykinin receptors are there? Which is predominant?

A

B1 and B2

44
Q

Which NO donors have an “intermediary” duration of action (how long is this)?

A

Oral/sustained-release NTG or isosorbide dinitrate

45
Q

What’s the chemical name of desmopressin?

A

1-diamino {D-Arg6] arginine vasopressin (dDAVP)

46
Q

Name the pharmacological actions of NO.

A
  1. Smooth m relaxation
  2. Decreased (white) cell adhesion
    1. Decreased E-selectin on endothelial surface
  3. Inflammatory response
  4. Neurotransmitter
  5. Platelet inhibitor
47
Q

How are angiotensin receptor inhibitors administered?

A

PO

48
Q

Name 2 angiotensin receptor inhibitors.

A

Losartin, valsartin

49
Q

Arginine is converted by NOS (+ NADPH and O2) to ________________ + NO.

A

Citrulline

50
Q

*What are the effects of NO within the cell?

A

Activates GC –> cGMP

  • Also generates several reactive nitrogen derivatives by interacting w/ O2 and superoxide radicals.
    • These oxides of nitrogen are highly reactive and unstable, interact with numerous proteins, lipids, nucleic acids and metabolize.
51
Q

Bosentin: indications?

A

Pulmonary HTN

52
Q

Icatibant: MoA?

A

Bradykinin (B2) receptor inhibitor

53
Q

What can convert HMW kininogen to bradykinin?

A

Plasma kallikrein

54
Q

What converts angiotensinogen to ang I?

What converts ang I to ang II?

What converts ang II to ang III?

A

Renin

ACE

Aminopeptidase

55
Q

Is L-NMMA selective or non-selective?

What about L-NAME?

(not that important)

A

Non-selective

Non-selective

56
Q

Icatibant: indications?

A

Inflammatory diseases, (hypotension, myocardial hypertrophy)

57
Q

How is desmoprssin administered?

A

IV

58
Q

Name all of the vasoactive peptides, if you can (7)

A
  1. Captopril, Enalapril
  2. Losartan, Valsartan
  3. Icatibant
  4. Desmopressin (DDAVP)
  5. Bosentan
  6. Omipatrilat, sampartilat, fasidotrilat
  7. Aprotinin (also thrombolytic)
59
Q

What nerves in the PNS release NO?

A

Nonadrenergic, noncholinergic (NANC)

  • E.g. erection
60
Q

Name 2 ACE inhibitors.

A

Captopril, enalapril

61
Q

Kininase II breaks down ______________.

Another name for this enzyme is _____________.

A

Kinin/bradykinin

ACE

62
Q

7-nitroindazole: MoA?

Is it selective or nonselective?

(not that important)

A

NO inhibitor. Competitive inhibitor–binds both tetrahydrobiopteran and arginine binding sites in NOS

Partially selective for NOS-1

63
Q
A
64
Q

Septic shock:

Bacterial infection and LPS B activate _________, resulting in hypotension, shock and possible death. This effect is reversed by NO inhibitors such as the L-NMMA.

A

iNOS (NOS-2)

65
Q

What is the MoA of N-monomethyl-L-arginine? (L-NMMA)

(not that important)

A

NO inhibitor

Competitive inhibitor–binds arginine binding sites in NOS

66
Q

Which NO donors have a “short” duration of action (how long is this)?

A

SL NTG or isosorbide dinitrate

(10-30 minutes)

67
Q

What is nitrous oxide used for? (N2O)

A

Gaseous anesthetic

68
Q

What is the MoA of N-nitro-L-arginine methyl ester? (L-NAME)

(not that important)

A

NO inhibitor

Competitive inhibitor, binds arginine binding site in NOS

69
Q

What drug is the most wide used donor of NO?

A

Nitrates (eg NTG)

70
Q

*Describe the cellular MoA of NO on smooth m.

A

A. NO interacts w/heme moeity of guanylyl cyclase

B. Increased production of cGMP

C. Dephosphorylation of myosin

71
Q

Potent interactions between NO donors and Viagra have been reported resulting in _____________.

A

hypotension

72
Q

What is the physiological purpose of NO release in the bv following injury?

A

NO counteracts the vasoconstriction process

73
Q

What’s another name for vasopressin?

Explain the physiological effects of vasopressin.

A

Anti-diuretic hormone, ADH

  • Long term control of blood pressure through its action on the kidney to increase water resorption.
  • It has short term vasoconstrictor actions.
74
Q

How are ACE inhibitors administered?

A

PO

75
Q

How could decreasing NO affect BP?

A

Increase BP

76
Q

What are 2 other names for ACE?

A

Peptidyl dipeptidase

* Kininase II

77
Q

Would NOS-3 be elevated or decreased in IBS, arthritis, and other inflammatory diseases?

A

Increased (excessive vasodilation)

78
Q

Hemaglobin: MoA?

A

NO scavenger

79
Q

What is the effect of endothelin?

How many isoforms are there?

How many AAs long is it?

A

Vasoconstriction

3

21

80
Q

Which NO donor has a “long” duration of action (how long is this)?

A

Transdermal NTG

(8-10 hrs)

81
Q

Describe the methods of administration of NO. (kind of a dumb flashcard, just read)

A
  • Commercial NO systems are available which can accurately deliver inspired NO concentrations between 0.1 and 80 ppm and simultaneously measure NO and NO2 concentrations.
    • intermittent or continuous delivery
  • NO can be administered via a closely fitted mask. It is administered mostly in the management of primary pulmonary hypertension.
    • After the administration, NO should be gradually discontinued to avoid complications such as rebound
82
Q

Icatibant: route of administration?

A

PO

83
Q

BBS-2: MoA?

Selective or non-selective?

(not that important)

A

NO inhibitor: Inhibits iNOS dimerization

Also weakly inhibits eNOS and nNOS

84
Q

What are 2 ways by which NO is deactivated?

A
  • Heme
  • Free radicals superoxide
85
Q

How does NO relate to the CNS, in terms of diseases implicated?

A

NO is implicated in neuromodulatory process and has impact on stroke and vascular dementia.

86
Q

Besides converting ANG I to ANG II, what else does ACE do?

Therefore, what other effects can ACE-inhibitors have

A

Breaks down kinins

Vasodilatory (due to lack of kinin breakdown)

87
Q

An elderly hypertensive hospitalized patient was treated with an ACE inhibitor, namely captopril. During hospitalization she became septic due to an infection. Soon after she went into severe hypotensive shock.

What is the likely cause of the hypotensive shock in this patient?

A

Pt’s ACE blocked, no ANG II produced (good). But blocking ACE blocks bradykinin breakdown, leading to excessive vasodilatory actions of bradykinin/kinins (bad).

88
Q

How is NO level altered in shock?

A

NO levels increased, markedly

Pharm (32 decks)

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