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Pharmacology > Nitric Oxide > Flashcards

Nitric Oxide Flashcards

1
Q

What are 3 actions of NO?

A

1) relax smooth muscle
2) decrease cell adhesion
3) evoke inflammatory response

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2
Q

Endogenous nitric oxide is generated from the oxidation of the ___________ group of __________.

A

guanidine group of arginine

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3
Q

True or false: exposure of LPS results in generation of NO in the macrophage

A

TRUE

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4
Q

When is NO normally, physiologically released by the endothelium?

A

upon stimulation with Ach and carbachol

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5
Q

What is the role of NO in the face of injury?

A

counteracts vasoconstriction

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6
Q

What enzyme family makes NO?

A

nitric oxide synthase

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7
Q

Which form of NOS is inducible?

A

NOS-2

inTWOcible

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8
Q

What does it mean to be for NOS to be inducible?

A

triggered by disease (like sepsis)

NOS-2 is in macrophages and smooth muscle cells

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9
Q

What are the 2 endogenous, normal NOS?

A

NOS-1 and NOS-3

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10
Q

Which NOS is also called eNOS (found in the endothelial cells)?

A

NOS-3

3 rhymes with e

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11
Q

Which NOS is the neuronal NOS?

A

NOS-1 (brain is #1)

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12
Q

What is the substrate for NOS?

A

L-arginine

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13
Q

What inhibits NOS?

A

arginine analogues (N-monomethyl L-arginine)

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14
Q

How does nitroprusside differ from nitroglycerin?

A

nitroprusside: spontaneously generate NO
nitroglycerin: require presence of thiol compound such as cysteine

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15
Q

What is the mechanism of action of NO?

A

interacts with heme moiety of soluble guanyl cyclase in cytoplasm of cell

guanyl cyclase converts GTP to cGMP

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16
Q

NOS converts arginine to ______________ and NO

A

citrulline

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17
Q

Once formed, NO can do what 2 things?

A

nitroslyate proteins (NO is a free radical) or complex with heme of guanylyl cyclase

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18
Q

The most stable form of nitric oxide is _____ and it is used as a measure for how much NO is produced

A

NO3

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19
Q

What inactivates NO?

A

heme and free radical superoxide

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20
Q

How does superoxide dismutase affect the duration of NO action?

A

prolongs it by scavenging superoxide, NO’s inactivator

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21
Q

How does glutathione play a role in NO regulation?

A

glutathione regulates peroxynitrile which is the product of NO and superoxide

peroxynitrile complexes with sulfhydral group of many key enzymes

WANT HIGH LEVELS OF GLUTATHIONE TO MITIGATE DANGEROUS NO FORMATIONS

22
Q

What are 4 ways to inhibit NO?

A

1) L-arginine derivatives (block formation of NO)
2) inhibitors of nitric oxide synthase
3) inhibitor of binding of arginine to NO
4) scavenger of NO

23
Q

What is the danger of excess production of NO?

A

generation of peroxynitrite which is toxic to cells

24
Q

Why are NO inhibitors important for the treatment of sepsis related disorders?

A

reduce formation of peroxynitrite

25
Q

NO’s major effects are mediated by the activation of _______ _______ which results in the generation of _______.

A

guanyl cyclase resulting in the generation of cyclic GMP

26
Q

In addition to activating guanylyl cyclase, NO can generate several reactive nitrogen derivatives by interacting with molecular radicals. Why are these oxides dangerous?

A

they are highly reactive and unstable and alter the physio disposition of cells and tissues

27
Q

The beneficial effects of NO are __________________, ___________, and _______________

A

smooth muscle relaxation
vasodilation
immune regulation

28
Q

The negative effects of NO are _____________

A

free radical formation, nitrosation, irritant effects

29
Q

Decrease NO can result in _____________ blood pressures

A

elevated

30
Q

What is the danger of NO interaction with sildenafil (viagra)?

A

viagra also increases cGMP by inhibiting phosphodiesterase (which converts cGMP to GMP) leading to massive amounts of cGMP/vasodilation

31
Q

True or false: NO is a potent inhibitor of WBC adhesion to the endothelial surface?

A

TRUE; decreases release of adhesion molecules such as E-selectin on endothelial surface

32
Q

True or false: NO can protect against ischemic and reperfusion injury

A

true

33
Q

What are the clinical applications of NO for the respiratory system?

A

improves cardiopulm function for patients with pulm hypertension

34
Q

What form of NO is given to patients with pulm hypertension?

A

INOmax

35
Q

What is responsible for producing hypotension in septic shock patients?

A

LPS activation of iNOS-2

36
Q

What reverses septic shock?

A

L-NMMA (NO inhibitor)

37
Q

What are the dangers of too much NO?

A

ischemia and perfusion defects

38
Q

How does atherosclerosis affect the formation of NO?

A

impairs it (plaques and endothelial damage block it) leading to increased cellular proliferation and exacerbating athero

39
Q

How can you treat the decreased NO formation in athero patients?

A

L-arginine and NO donors (like nitroprusside and nitroglycerin)

40
Q

What effect does NO have on platelets?

A

inhibitor of platelet adhesion, activation, aggregation

41
Q

How can NO be used in organ transplants?

A

acts a cytoprotective agent to prevent cellular and platelet adhesion in new grafts (since accelerated graft atherosclerosis after transplant is a major cause of graft failure)

42
Q

Why are graft patients recommended to be on dietary arginine supplements?

A

arg is a substrate for NOS and increases NO formation which prevents cellular adhesion and accelerated graft athero

43
Q

What is the relationship between NO and the PNS?

A

nonadrenergic, noncholinergic neurons release NO which assists erectile responses

44
Q

Viagra + NO donors is a dangerous combo because it causes massive ___________

A

hypotension

45
Q

Which NOS is associated with acute inflammation found in IBD, arthritis, etc?

A

NOS-3

46
Q

What are the 3 NO donor drugs?

A

1) nitroglycerin
2) isosorbide dinitrate
3) amyl nitrates

47
Q

What is the longest acting of the NO donor drugs?

A

nitroglycerin (transdermal)

48
Q

What is the shortest acting NO donor?

A

inhaled amyl nitrate
sublingual nitroglyc
isosorbide dinitrate

49
Q

How does an increase in cGMP lead to vasodilation?

A

dephosphorylation of myosin

50
Q

inhaled NO is administered mostly in the management of _______________________

A

primary pulm hypertension

Pharmacology (21 decks)

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