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Phcol 401 > Quiz #1 Material > Flashcards

Quiz #1 Material Flashcards

1
Q

Pharmacodynamics vs. Pharmacokinetics

A
  • Pharmacodynamics: Effects of drug on body
    • Receptor binding, signaling, agonism/antagonism, dose-response curve, physiological effect
  • Pharmacokinetics: Effects of body on drug
    • ADME
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2
Q

Drug Size

A
  • Majority with MW 100-1000
  • Too small: insufficient selectivity at target site
  • Too large: poor absorption and distribution in the body
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3
Q

Receptors

A
  • Interact with drugs to cause change in biological system
  • Only care about those with drug specificity
  • Conformational change
  • Cascade of events
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4
Q

Example of Receptor: Ach receptors

A
  • 5 subunits (two alpha, beta, delta, gamma)
  • Ach bind to the two alpha subunits
  • Conformational change to allow for Na+ to flow through
  • Small molecule (Ach) binds to a large macromolecule (Ach receptor)
  • Cause conformational change in the large receptor
  • Results in physiological effect (muscle contraction)
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5
Q

Effectors:

A
  • Translate drug binding into change in cellular activity
  • Often enzymes (kinase, phosphodiesterase, etc.)
  • _Can be part of recepto_r:
    • Insulin receptor: Tyrosine kinase is part of receptor
    • Nicotinic acetylcholine receptor: Ion channel that functions as the effector
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6
Q

Receptor Types:

A
  • Proteins: bind hormones/neurotransmitters, channels, enzymes
  • Nucleic acids
  • Membrane lipids
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7
Q

Protein Receptor Signaling Mechanisms:

A
  • Nuclear receptors (intracellular): steroid hormones, estrogen, vitamin D
  • Kinase linked receptors: growth factors, cytokines (phosphorylate proteins)
  • Ion channels: acetylcholine, glutamate
  • GPCRs: histamines, opioids, serotonin
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8
Q

Properties of Drug-Receptor Interactions:

A
  • Multiple sites where drug-receptor interact
  • Short range interactions
  • Specific interactions between chemical groups on drug and receptor
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9
Q

Relative strengths of Drug-Receptor Interactions

A

Strongest: Covalent, Ionic, Hydrogen, Hydrophobic, Van de Waals: Weakest

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10
Q

At least how many points of contact between a drug and receptor are required to see a difference in isomer activity?

A

Three. With 2 you can flip bonds.

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11
Q

Enkephalin and Morphine have similar regions that can interact with opiate receptors. More interactions means that there will be a more potent drug. How chemical groups are presented to a receptor determines how a drug will work.

A
  • N-methyl piperidine is an essential feature
  • Oxygen at C3 is essential
  • Oriented cleft in piperidine ring
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12
Q

Extracellular Messengers

A

Circulating hormones, neurotransmitter, cytokines, etc.

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13
Q

Animal Cells Communicate via Circulating Hormones

A
  • Hormones are synthesized, stored for secretion, secreted, and induced biophysical/physiological change at target cells
  • Secretion and degradation are regulated
  • Feedback inhibition at synthesis, storage and secretion steps
  • Drug can interfere with signaling sometime within these steps.
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14
Q

General Receptor Coupling Mechanisms (4)

A
  • Two Messenger System:
    • Receptor coupled to an effector system that changed intracellular concentration of 2nd messenger
    • Usually an enzyme
    • Usually; 1st messenger→effector→2nd messenger→protein kinase cascade
  • Ion Channel Coupled Receptors:
    • Receptor directly coupled to/is an ion channel
    • Response time fast because no intervening messenger (milliseconds)
  • Steroid Hormone Receptors
    • Hormone crosses to a membrane and binds intracellular with receptor
    • Hormone:Receptor complex goes to nucleus to regulate gene transcription
    • Response elements in gene promoters
  • Receptor Kinases/Phosphotases or other enzymatic activity
    • Receptor is a kinase
    • When activated, initiated protein kinase cascade
    • No intermediate, diffusible messengers
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15
Q

Two Messenger Systems:

A
  • Extracellular message (hormone or neurotransmitter) never enters the cell
  • The second messenger concentrations are changed within the cell after receptor activation
  • 2nd messenger can increase or decrease from a signal
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16
Q

Regulatory Advantages of Second Messenger Systems (5):

A
  • Without entering cell
  • Fast reponse/termination
  • Amplification
  • Multiple inputs onto one 2nd messanger
  • Cross-talk between different signal transduction systems
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17
Q

Common Second Messengers:

A
  • cAMP: First one described; autonomic, CNS and endocrine; all types of physiology
  • cGMP: vision, smooth muscle contraction,
  • Ca2+: universal (prokaryotes as well); autonomic and CNS
  • Phosphoinositide breakdown products; IP3
  • Arachidonic acid derived from lipids
  • NO, nitric oxide: diffuse across cell membranes from one cell to another
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18
Q

What is the pharmacological significance of the two-messenger system?

A
  • Drugs can affect the concentration of intracellular 2nd messengers
    • Beta-adrenergic receptors coupled to adenylyl cyclase, action mediated through cAMP. Beta agonist/antagonist modify cAMP
  • Understanding mechanism of 2-messenger system is crucial for understanding how drugs work
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19
Q

The Structure of cAMP:

A
  • Synthesized from ATP
  • 3’, 5’ cyclic adenosine monophosphate
  • Sutherland in 1957 studying glycogen breakdown in liver and muscle
    • Adrenaline→^cAMP→glycogen breakdown
  • Adenylyl cyclase catalyzes formation of cAMP
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20
Q

Physiological Processes Controlled by cAMP: (in all cells except for erythrocytes)

A
  • Glycogenolysis: stimulates breakdown of glycogen (use stored energy)
  • Gluconeogenesis: inhibits synthesis of glycogen
  • Lipolysis: stimulates breakdown of triglycerides
  • Secretion of neurotransmitters: generally stimulates secretion
  • Ion channel activity: activates ion channels
    • Either directly or through cAMP-dependent protein kinases (ex: glutamate AMPA receptors)
  • Muscle contractility: stimulates cardiac muscle stimulant: adrenaline→^cAMP→heart rate
  • Growth: antiproliferative
  • Differentiation: stop proliferating so they can differentiate
  • Gene transcription: CRE (cAMP response element) in promoters, long term memory
  • Memory formation
  • Melatonin synthesis from serotonin regulated by cAMP
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21
Q

cAMP is Synthesized from ATP:

A
  • Catalyzed by adenylyl cyclases
    • In cytoplasmic membranes
    • Regulated by receptors and intracellular protein kinases
  • ATP→cAMP+ PPi (uses Mg2+) cofactor
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22
Q

Synthesis and Degradation of cAMP

A
  • Degradation: cyclic nucleotide phosphodiesterases
    • cAMP to 5’-AMP
  • PDE with different tissue distributions and regulatory properties
    • Common drug target site
    • Inhibit PDE, Increase [cAMP]
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23
Q

Synthesis and Degradation of cGMP:

A
  • Similar to cAMP
  • Guanylyl cyclases to form cGMP from GTP
  • PDE to degrage cGMP
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24
Q

Structure of Xanthenes and Methylxanthines:

A
  • Two mechanisms to increase cAMP
    • Inhibit PDE and elevate cAMP levels
    • Stimualate adenosine receptors that are coupled to stimulation of AC
  • No methylation→3 methyl
    • xanthine, theobromine, theophylline, caffiene
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25
Q

Viagra Increases Penile Erection by Increasing cGMP:

A
  • Viagra: potent and selective PDE5 inhibitor
  • cGMP promotes smooth-muscle relaxation, blood flow, erection enhancement
  • Inhibiting PDE5 increases cGMP concentrations
  • Originally for BP due to vasodilator properties
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26
Q

Different Types of cAMP Transients Used for Signaling:

A
  • High cAMP levels are toxic
  • Want transient cAMP levels
    • Shape and duration encode specific information
      • (Example: signaling to nucleus for transcription require more robust or prolonged cAMP increases)
  • Olfactory: oscillating cAMP
  • Mechanisms to rapidly produce in a local area and then degrade
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27
Q

The cAMP Signal Transduction System:

A
  • Agnosists (peptide hormones, catacholamines, muscarinic agonists and neurotransmitters) to receptors to influence AC (adenylyl cyclases)
  • cAMP activates protein kinases to phosphorylate proteins and modulate their activity
    • Exception: Olfactory epithelium
      • CNG-cyclic nucleotide gated ion channels
      • Opens ion channels without protein kinases
  • Specificity is dictated by receptors on cells.
  • Cells will have multiple types of receptors coupled to the stimulation or inhibition of adenylyl cyclases
  • 1st messenger doesn’t need to enter the cell to cause physiological effects
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28
Q

PKA Reaction:

A
  • Discovered by Krebs and Fischer at UW
  • Regulatory (R) and catalytic (C) subunits
  • R is inhibitory
    • cAMP:R→R:cAMP complex dissociates from PKA→C is activated
  • Need R to dissociate for PKA to work
    • cAMP causes R to dissociate
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29
Q

Protein Phosphatases and the cAMP Regulatory System:

A
  • Phosphatases “undo” actions of PKA
    • Ex: calcineurin is a Ca2+ stimulated enzyme
      • Calcinerurin catalyzes deP of AMPA receptors, decreases synaptic transmission
  • Signal terminated by dephosphorylation/decreased levels of 2nd messenger
  • cAMP regulatory system works in vivo
30
Q

Different Types of Protein Kinases:

A
  • cAMP-dependent protein kinases (PKA)
  • cGMP-dependent protein kinases (PKG)…vision
  • Calcium regulated kinases:
    • Myosin light chain kinases: smooth/skeletal muscle
    • Phosphorylase kinase (also cAMP regulated)
    • Calmodulin stimulated protein kinases
      • Bind Ca2+ and stimulates calmodulin-dependent protein kinases
    • PKC
      • Regulated by DAG and Ca2+
  • Receptor tyrosine kinases
    • Growth, proliferation and differentiation
31
Q

Number of Protein Kinases:

A
  • Lots have recently been discovered
  • 500 different types in human, not all are seen in one cell type
32
Q

Dendrogram of 491 PK domains from 478 genes:

A

Different classes of protein kinases and close to 500 in humans

33
Q

cAMP Activation of Glycogenolysis and Inhibition of Glycogen Synthesis

A
  • Catecholamines liberate glucose in skeletal muscle and liver
    • Liver: 2nd messenger is Ca2+
    • Skeletal: 2nd messenger is cAMP
  • Epinephrine or glucagon
    • ATP→(AC)→cAMP→(PDE)→3’,5’AMP
      • cAMP activates PK
        • Phosphorylates glycogen synthase to inactivate it
        • Phosphorylates phosphorylase kinase to activate it
          • Phosphorylates phosporylase kinase b to activate it
  • Kinases leads to amplification
  • Rapid generation of free glucose in “fight or flight”
  • Depletion of glycogen not significant in endurance exercise using large muscle groups
  • Liver responsible for maintaining glucose concentration in bloodstream
    • Ca2+ stimulates phosphorylase kinase
  • Phosphorylase kinase activity differs between cell types
34
Q

cAMP and Lipolysis (Fatty Acid Metabolism)

A
  • Hormones and catecholamine’s stimulate AC to increase cAMP in fat cells
  • ^cAMP→stimulate PKA→phosphorylate lipase/activate it
    • Lipase breaks down TG to FA and glycerol
    • Methylxanthense stimulate this by inhibit PDE and activating AC
  • Beta-blockers
    • Block adrenaline activation, but not peptide hormone (glucagon), activation of fat adenylyl cyclases…different receptors
35
Q

Type 3 Adenylyl Cyclase Activity is required for Leptin Sensitivity:

A
  • (-)AC3, obese
  • Not because deficient in lipolysis, but rather leptin insensitive
  • Fat secrete leptin→leptin receptors in hypothalamus to decrease hunger/food consumption
    • Leptin:leptin receptors→form alpha-MSH→MC4-R+cAMP→appetite suppression
      • MC4-R coupled to AC3
    • Transcriptional process
36
Q

Some Neurotransmitter Receptors Regulate cAMP

A
  • Beta and alpha adrenergic, dopamine, norepi, serotonin, muscarinic, histamine
  • Norepi, dopamine, serotonin, muscarinic coupled to AC in neurons
  • cAMP produced modulates ion channel activity, increases neurotransmitter release and increases in transcription
  • cAMP→PKA→ion channel effects
    • CNG channels in brain that are directly gated by cAMP
37
Q

cAMP Oscillates During the Heart Contraction Cycle:

A
  • E and NE (catecholamines) stimulate contractility w/ positive inotropic and chronotropic effects in heart
    • Activate beta-adrenergic receptors in myocardium coupled to AC activation
  • Cyclical cAMP parallels contraction cycle
    • Regulate contraction cycle w/o adrenergic stimulation
38
Q

cAMP Mediates Olfaction:

A
  • Odor/Pheremone receptors coupled to stimulation of AC
  • cAMP opens Na+ specific channel. cGMP also regulates ion channels in sensory cilia
39
Q

cAMP Stimulates Transcription through CRE (cAMP Response Element):

A
  • cAMP-PKA phosphorylates TF (CREB)
  • P-CREB to CRE in DNA to stimulate transcription
  • CREB transcription in long-term memory
40
Q

cAMP and Human Disease:

A
  • Tumors
  • Psoriasis: rapid proliferation of skin cells
  • Pseudohypoparathyroidism: defects in hormone response b/c defect in hormone coupling system (receptor→AC disrupted)
  • Bacterial toxins: increase cAMP
  • Depression
  • Obesity
  • Graves Disease
41
Q

Graves Disease:

A
  • Ab to activate TSH
  • TSH receptor coupled to AC; cAMP stimulates release of thyroid hormone
  • Ab→^TSH→^cAMP→^thyroid hormone→goiter
42
Q

Intracellular Free Calcium is Tightly Regulated:

A
  • Ca2+ controls: secretion, metabolism, muscle contraction, cell shape, growth, proliferation, cell survival, synaptic plasticity, and transcription
  • Normal [intracellular Ca2+]=100nM
    • Pumped into ER, mitochondria, or out of cell
  • Extracellular Ca2+=mM
    • Intracellular increase from 0.1uM to 10 uM
  • Ca2+ Channels: allow extracellular calcium to enter
    • Voltage gated (neurons and heart)
    • NMDA glutamate activated channels
      • Need glutamate AND depolarization
43
Q

Receptors Coupled Through Phospholipase C Increase Intracellular Free Calcium

A
  • PLC breaks down PIP2 into IP3 and DAG
    • IP3 binds to IP3 receptor and releases Ca2+ from ER membrane
    • Ca2+ can then regulate PKC and calmodulin
44
Q

(calmodulin) CaM-Regulated Proteins:

A
  • Enzymes:
    • Cyclic nucleotide PDE
    • AC
    • ATP-dependent Ca2+ pumps
    • Myosin light chain kinase
    • CaM kinase I, II, and IV
    • Phosphorylase kinase
    • Calcineurin
    • NO synthase
    • RasGRF1, a CaM-activated GEF
  • Nonenzymatic Proteins:
    • Tubulin
    • Troponin I
    • Spectrin, fodrin, caldesmon, calspectin, cytosynalin
    • MAP-2 and Tau
    • Neuromodulin and Neurogranin
    • Ca2+ channels
45
Q

Calmodulin Structure:

A
  • 4 Ca2+ binding sites
  • Ca2+ to CaM→exposes hydrophobic domain on CaM→enhances affinity for its target protein
46
Q

The phospholipase A2/Arachidonic pathway:

A

Agonists (serotonin and dopamine subclasses)→Receptors (GPCR)→PLA2→AA (2nd messenger)→Prostaglandin

47
Q

General Properties of Adenylyl Cyclase

A
  • Catalyze formation of cAMP from ATP
  • Km=0.1mM
  • Intracellular [ATP]=several mM
  • Enzyme saturated; regulated by turnover rate
  • Different adenylyl cyclases have different regulation, tissue and subcellular distributiona
48
Q

Adenylyl Cyclases in Membranes:

A
  • 12 transmembrane domains and 2 cytoplasmic loops by hydropathy analysis
  • Recombinant without transmembrane domains has catalytic activity regulated by G protein
    • Cytoplasmic loops=catalytic activity
    • Stimulated by forskolin; drug that binds to C domain
  • Function of transmembrane domains?
    • 1) Ion channel? Pump cAMP out of cell to finish signal?
    • 2) Membrane anchoring/subcellular location?
    • 3) Voltage sensitivity (seen in hippocampal and cortical neurons)?; Have charged amino acids. Or are they associated with voltage-sensitive protein?
49
Q

Structure of the C1 and C2 domains of adenylyl cyclase:

A
  • Two G-coupling proteins, Gi and Gs, bind to catalytic domains
  • Forskolin, from plants, binds C domains
    • Promote interaction between C1 and C2
50
Q

Adenylyl Cyclase Regulatory Mechanisms: (How to Regulate AC)

A
  • Stimulation by Gs-coupled receptors:
    • Gs and Gi proteins couple stimulatory and inhibitory proteins to specific AC
    • Ex: B-adrenergic in heart/resp. smooth muscle coupled to stimulation of AC through Gs→relaxation/vasodilation
  • Inhibition by Gi-coupled receptors:
    • Ex: Muscarinic receptors inhibit AC and depress cAMP
    • A2-adrenergic receptors also inhibit AC through Gi
  • Stimulation by PKC
  • Inhibition by PKA
    • *Feedback inhibition*
    • cAMP increases→activates PKA→deactivates AC
    • Ex: AC5
  • Calcium stimulation mediated through calmodulin
    • Required for consolidating/memory formation
    • Ex: AC1 and AC8
  • Calcium inhibition AC3
    • Ex: Mediated through CaM Kinase II phosphorylation of AC3
  • Calcium inhibited AC in olfactory system
    • PDE stimulation and inhibition of AC
  • Voltage sensitivity
  • Stimulation or Inhibition by the beta/gamma complex of G-coupling proteins
    • Ex: AC2 and AC4 are stimulated by beta/gamma
51
Q

Hormone Regulation

A
  • Tissue specificity of AC
  • Heart: Beta-adrenergic receptors stimulation of AC, muscarinic receptor inhibition of AC
  • Liver: Glucagon and beta-adrenergic receptors are coupled to stimulation of AC
  • Adipose: 7 receptors coupled to stimulate AC
52
Q

Multiple receptors can couple to a single AC catalytic subunit:

A
  • Non-additive effects
  • Multiple receptors to a single catalytic subunit
53
Q

Membrane fusion experiment:

A
  • Cell with receptor only and cell with AC only showed no hormone-stimulated AC activity
  • Fused membrane had activity
54
Q

Glucagon Dose Response:

A

Agonist binding corresponds quantitatively with stimulation of AC

55
Q

Beta-Adrenergic Agonist Dose Response Curve:

A
  • Interactions of agonists with their receptors are specific
  • E and NE curve similar but not the same
  • Different isoforms of isoproterenol have very different curves
  • Receptor interactions have high affinity and very specific
56
Q

Beta-agonists and antagonists:

A
  • Binding of drugs is necessary but not sufficient for stimulating AC
  • Agonist binding→conformational change→activate receptor
  • Antagonist→high binding energy→no conformational change→energy lost as heat
57
Q

Receptor Mechanisms:

A
  • Receptor stimulation of AC by hormones, neurotransmitters or catecholamine’s requires 3 protein substrates:
    • Stimulatory receptor, Rs
    • Gs
    • C subunit of AC
  • Receptor inhibition of AC by hormones, neurotransmitters or catcholamine’s requires 3 protein substrates:
    • Inhibitory receptor, Ri
    • Gi
    • C subunit of AC
  • Need:
    • (1) Receptor (Rs or Ri)
    • (2) G protein (Gs or Gi)
    • (3) C subunit of AC
58
Q

Adenylyl cyclase active when GTP bound to Gs:

A
  • Gs and Gi active when have GTP bound
  • Have intrinsic GTPase activity
  • GTP→GDP inactivates G-protein activity
  • Hormone receptors complexed to receptors are GEF (guanylyl nucleotide exchange factors)
    • GTP→GDP bound to G-coupled proteins
    • Increases off rate of GDP from G-coupled proteins so that GTP can bind
59
Q

Heterotrimeric structure of Gs and Gi:

A
  • 3 subunits in G protein: alpha, beta and gamma
  • Alpha subunits are GTPase activity
  • Beta/gamma inhibit alpha
  • GTP binds alpha→beta/gamma dissociate→alpha activated→stimulates AC activity (Gs) or inhibition AC activity (Gi)
  • Beta/gamma shuffles between Gs and Gi
    • Coordinated regulation
60
Q

Model for G protein Activation:

A
  • Alpha subunits has GDP bound and beta/gamma associated→inactive
  • Receptor/agonist complex (GEF) catalyzes exchange of GTP→GDP to phosphorylate GDP bound to alpha subunit
  • GTP bound alpha subunit causes beta/gamma to dissociate
  • G-alpha then interacts to activate Gs or Gi
  • G protein allows multiple receptors to influence enzyme
    • Are the shuttle between receptors and ACs
61
Q

Symmetry for G protein regulation of AC:

A

When Gs is activated beta/gamma dissociate and then inhibit Gi

62
Q

Cholera Toxin and Gs:

A
  • ADP-ribosylation of Gs-alpha
    • Inactivates GTPase activity
  • Permanently activated
  • High cAMP→diarrhea
63
Q

Pertussis Toxin:

A
  • ADP-ribosylation of Gi-alpha
    • Inactivates Gi
  • Increases cAMP
    • Neutralizes immune response in lungs
  • Pertussis also makes its own small AC that invades lungs and increases cAMP
64
Q

Anthrax Adenylyl Cyclase:

A
  • Invasive cAMP
    • Activated by calmodulin
  • If lacking AC, avirulent
  • Edema factor
65
Q

Vibrio vulnificus biotype 3 toxin is an AC toxin essential for virulence in mice:

A

Invasive AC

66
Q

Pseudohypoparathyroidism

A
  • Unresponsive to parathyroid and other hormone that normally couple to AC stimulation
  • Low cAMP levels
  • Mutated Gs
67
Q

Pituitary and Thyroid Tumors:

A
  • GHRH→GHRH receptor→Gs→AC→cAMP→GH
  • Mutation in Gs-alpha, lose GTPase activity, high cAMP levels, uncontrolled growth
68
Q

Analogy between transducin and Gs

A
  • cGMP interacts with sodium channel in rod to open them
    • cGMP lowered by PDE, channel closes
  • Transducin is like Gs and Gi
    • Activates PDE
69
Q

Model of the transducin/visual signaling system:

A

Signal: light, receptor:rhodopsin, G-protein:transducing, effector system:cGMP PDE, second messenger is cGMP

70
Q

How many G-coupling proteins?

A
  • Hundreds of cell receptors are GPCR
  • 20 different G-coupling proteins (Gs, Gi, Gt, Go)
71
Q

G proteins have common transmembrane topology:

A

All GPCR to G-proteins have 7 transmembrane domains

72
Q

Examples of GPCR:

A
  • Vary in molecular size
  • 7 transmembrane domain, extracellular NH2/intracellular COOH

Phcol 401 (10 decks)

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