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PHARM 203 > Lecture 13 Nitric Oxide & H2S > Flashcards

Lecture 13 Nitric Oxide & H2S Flashcards

1
Q

How is Nitric Oxide Formed

A

From L-arginine and Oxygen

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2
Q

What else is Nitric Oxide known as

A

EDRF

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3
Q

Nitric Oxide Synthase (NOS)

A
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4
Q

What are the three different enzymes

A

Endothelial (eNOS)
Neuronal (nNOS)
Inducible (iNOS)

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5
Q

Endothelial (where)

A

Constitutive
Endothelial Cells
Leukocytes
Platelets
Mast Cell

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6
Q

Neuronal (where)

A

Constitutive
Neurons (CNS & PNS)
Mast Cells

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7
Q

Inducible (where)

A

Inducible (By inflammation stimulus)

Macrophages
Neutrophils

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8
Q

Which isoform of Nitric Oxide Synthase generates the most NO

A

Inducible

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9
Q

L-arginine-NO Pathway (Process that activates NOS)

A

Ach, bradykinin, substance P, etc activates receptor –> Releases more calcium –> Activates Calmodulin –> Activates an inactive NOS (Mechanical Shear Stress also contributes to activation) in Endothelial cells

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10
Q

L-arginine-NO Pathway (Process that activates GC)

A

Active NOS converts Arginine + O2 into Citrulline + NO –> NO activates Guanylyl Cyclase in smooth muscle cells

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11
Q

L-arginine-NO Pathway (Process that causes relaxation)

A

Active Guanylyl Cyclase converts GTP into cGMP –> cGMP causes relaxation

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12
Q

What kind of dimers are NOS isoforms

A

Homodimers

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13
Q

What cofactors are required for Constitutive Isoforms

A

NADPH
Flavin Adenine Dinucleotide
Flavin Mononucleotide
Heme
TH4
Ca2+/Calmodulin

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14
Q

What cofactors are required for Inducible Isoforms

A

NADPH
Flavin Adenine Dinucleotide
Flavin Mononucleotide
Heme
TH4

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15
Q

NADPH (NO Function)

A

Source of electrons

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16
Q

FAD/FMN

A

Takes electrons from NADPH and gives it to heme domain

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17
Q

Heme

A

Heme Domain takes electron from FAD/FMN

Also facilitates dimer formation

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18
Q

Ca2+/Calmodulin

A

Facilitates the transfer of electrons

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19
Q

Tetrahydrobiopterin (TH4)

A

Facilitates dimer formation

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20
Q

What does NO effect

A

Binds other enzymes that contain heme
S-Nitrosylation to thiol groups
Cysteine
Glutathione
Albumin
Deamination of DNA bases

Converts GTP into cGMP

21
Q

What does cGMP do

A

Sends signals further downstream activating:
Ion Channels - Cyclic nucleotide gated
Protein Kinases - Phosphorylates other things
Phosphodiesterases - Increase/Decrease cAMP

22
Q

How is cGMP signalling terminated

A

PDE5 converts cGMP into 5’GMP

23
Q

How is NO inactivated

A

Binding Hemoglobin

Formation of nitrate and nitrile

Formation of peroxynitrite

24
Q

Does NO have a long or short half life?

A

Short

25
Q

What happens in binding of hemoglobin inactivation

A

Hb(Fe-O2) binds to NO

26
Q

What happens in formation of nitrate and nitrite inactivation

A

NO reacts with Oxygen to form more stable compounds

27
Q

What happens in formation of peroxynitrite inactivation

A

NO reacts with free radicals

Highly reactive can cause some damage

28
Q

eNOS (effects)

A

Vascular

Decreases peripheral vascular resistance
Decreases blood pressure
Platelet Inhibition

29
Q

eNOS (What activates it)

A

Ca2+ activated calmodulin, more Ca2+ means more activity

Fluid shear stress can act as stimuli to cause activation

Regulated by phosphorylation and are always active

30
Q

nNOS (general effects)

A

Neuronal

31
Q

nNOS (CNS effects)

A

Neurotransmitter

Learning and memory formation

32
Q

nNOS (PNS effects)

A

Non-Adrenergic Non-Cholinergic (NANC) Neurotransmitter

Neurogenic Vasodilation
GI, Respiratory, Genital, Urinary Functions
Autonomic Innervation of Smooth muscle

33
Q

nNOS (Neuroendocrine Effects)

A

Regulates/Influences:
Reproductive Behaviours
Aggression
Feeding

34
Q

iNOS (effects)

A

Non-Specific Host Defence Mechanism

Expressed in response to bacterial endotoxins

35
Q

Regulation of iNOS

A

Regulated at the transcription level

36
Q

iNOS mechanisms of defence

A

Nitration of nucleic acids
Binding of Heme Enzymes
Binds mitochondrial enzymes that are needed for respiration

37
Q

Where are iNOS constitutively expressed

A

Kidney, Liver, Lung

38
Q

What inhibits iNOS expression

A

Glucocorticoids

39
Q

Excess iNOS, how to treat?

A

Inflammatory Conditions (Meningitis, Rheumatoid Arthritis)

No clinical drugs

40
Q

Glyceryl Trinitrate (Nitroglycerin)

A

NO Donor
Activates Smooth Muscles, Increase cGMP

Decrease Heart Rate

41
Q

Nitroprusside

A

NO Donor

Decrease Heart Rate

42
Q

Nebivolol

A

Selective beta 1 antagonist
Increases NO production

Decrease Heart Rate

43
Q

Statins

A

Lowers Cholesterol
Increase NO production

Decrease Heart Rate

44
Q

Sildenafil

A

PDE5 Inhibitors

Prevents termination of cGMP
This inhibition causes vasodilation –> Increases Blood Flow

45
Q

Tadarafil

A

PDE5 Inhibitors

Prevents termination of cGMP
This inhibition causes vasodilation –> Increases Blood Flow

46
Q

How do newborns handle pulmonary hypertension

A

Inhale NO to lower blood pressure

47
Q

Carbon Monoxide

A

At low concentration has vasodilator effects

Role in CNS

Produced by heme oxygenase

48
Q

Hydrogen Sulfide

A

At low concentrations has vasodilator and anti-inflammatory effects

Produced from cysteine

49
Q
A

PHARM 203 (19 decks)

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