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PCTH. 325 > Pharmacology MT > Flashcards

Pharmacology MT Flashcards

1
Q

Pharmacology is the study of ______ that interact with ______ through ________ process

A

Pharmacology is the study of substances that interact with living systems through chemical process

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2
Q

define medical pharmacology

A

the study of substances used to prevent, diagnose and treat disease

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3
Q

_______ is the study of undesirable effects of chemicals on living systems & ecosystems

A

toxicology

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4
Q

medical pharmacology studies _____ where as toxicology studies _____`

A

efficacy; side effects

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5
Q

Drug –> body is studied via __________

A

pharmacodynamics

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6
Q

body –> drug is studied via _________

A

pharmacokinetics

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7
Q

________ is the science of drug preparattion. and medical use of drugs in roman times (after 2500 BC)

A

materia medica

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8
Q

Francois Magendie & Claude Bernard are known for ..

A

developing methods of experimental physiology and pharmacology

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9
Q

The relation of an individuals genetic makeup to their response tot specific drugs is called _________

A

pharmacogenetics

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10
Q

What are 3 advances from the field of pharmacogenetics?

A
  1. understanding that certain diseases are inherited
  2. genomes of humans, animals and plants have been decoded - options for new research and treatment
  3. genetic techniques - gene therapy, KO mice
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11
Q

A new drug compound requires the discovery of a new ___________ (i.e the pathophysiological process or substrate of a disease condition)

A

new drug target

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12
Q

What occurs in in vitro studies and how long does it typically take?

A

Biological products and/or chemical synthesis, optimization (enzymes etc.) combine to form a lead compound.
~ 2 yrs

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13
Q

What is evaluated during animal testing? What occurs directly after?

A

Animal testing is the best model of disease for evaluating efficacy, selectivity and mechanism
- directly after: submit to a regulatory body = investigational new drug
~ 2 yrs

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14
Q

What does phase 1 of clinical testing evaluate? how many subjects?

A

Is it safe? Pharmacokinetics
20-100 subjects

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15
Q

What does phase 2 of clinical testing evaluate? how many subjects?

A

Does it work in patients w/ disease?
100-200 pt.

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16
Q

What does phase 3 of clinical testing evaluate? how many subjects?

A

does it work, double blind? (need significant effect)
randomized control trial
1000-6000 pt.

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17
Q

the clinical testing phase of drug development takes _- _ years

A

3-4 years

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18
Q

______ is an activator of biochemical pathway that mimics endogenous signalling

A

agonist

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19
Q

_________ stabilize receptors in an inactive form by shutting down constituent receptor

A

inverse agonist

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20
Q

______ inhibits a biological pathway by blocking endogenous signalling.

A

antagonist

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21
Q

_______ antagonist compound loosely binds to the same site as the natural ligand and inhibits natural action of ligand

A

competitive

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22
Q

_______ antagonist compound binds to _______ on the receptor and inhibits function

A

noncompetitive

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23
Q

_______ antagonist causes covalent modification of receptor

A

irreversible

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24
Q

Agonists and Antagonists require ___________ to induce change

A

target molecule (receptor)

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25
Q

a partial agonist increases ______ (compared to normal) but decreases ______ (compared to full agonist)

A

effect; effect size

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26
Q

Most rapid onset is the characteristic of ______ route drugs

A

IV

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27
Q
  • large volumes often feasible
  • may be painful
  • used for when you cant take meds on daily basis describes which drug route
A

intramuscular

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28
Q

Smaller volumes than IM - may be painful is the characteristic of ______ route drugs

A

Subcutaneous (SC)

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29
Q

most convenient route with a significant first past effect is the characteristic of ______ route drugs

A

Oral (PO)

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30
Q

Less first pass effect than PO is the characteristic of ______ route drugs

A

Parenteral Rectal (PR)

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31
Q

Often very rapid onset (2nd to IV) is the characteristic of ______ route drugs

A

inhalation

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32
Q

Slow absorption used for lack of first pass effect and prolonged duration of action is the characteristic of ______ route drugs

A

Transdermal

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33
Q

The fact that drugs exist in the form of organic and inorganic compounds is important for _______

A

how the body handles the drug

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34
Q

Drug size is an important factor for ______

A

administration

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35
Q

rational drug design describes …

A

design based on known structure of ligand & receptor

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36
Q

Allosteric Activator + Agonist = ______ response

A

max

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37
Q

Agonist + Competitive inhibitor = _____

A

Right shift - same max response but don’t increase max effect

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38
Q

Agonist + Allosteric inhibitor = ______

A

decrease below the use of a competitive inhibitor

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39
Q

What occurs when an agonist binds to a receptor

A

electrostatic changes = conformational change of receptor
ex. GPCR opening ion channel

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40
Q

4 process that are involved in termination of drug action

A
  1. dissociation of drug from receptor = terminate effect (ex. ionotropic receptor)
  2. action persists after drug has dissociated (ex. GPCR, phosphorylation)
  3. covalent bond - drug receptor complex must be destroyed and new receptors synthesized
  4. desensitization mechanisms - receptor mineralization
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41
Q

How do receptors determine the drug dose/ conc. & the effect

A

dose/conc: receptor affinity for a drug
effect: total # of receptors

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42
Q

____ is the maximal response that can be produced by a drug

A

Emax

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43
Q

____ is he concentration of drug that produced 50% of maximal effect

A

EC50

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44
Q

What is the eqn for the effect observed at conc. C

A
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45
Q

Constitutive activity describes… and is inhibited by ______

A

…the fact that some receptors are active w/o being bound to endogenous ligands.. inhibited by inverse agonist

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46
Q

____ can be used to measure he potency between different drugs in a log scale

A

EC50 - the drug conc.(on x axis) which induces a 1/2 max effect (Emax) response

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47
Q

responses to low doses usually _____ in _____ proportion to dose. Response increment _______ as dose increases

A

increase ; direct ; diminish

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48
Q

How do we chose among drugs and determine appropriate dosing? (2)

A

• pharmacologic potency (position dose axis)
• maximal efficacy (end point on response axis)

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49
Q

the maximum effect is driven by …. and reduced by increasing the concentration of _____

A

..the total # of receptors activated ; antagonist

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50
Q

Low doses of antagonists affect the agonist concentration effect curve by _______ whereas high dose antagonists cause it to _______

A

shift to the right ; reduce max response and R shift

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51
Q

EC50 is the dose required for ______ to experience 50% ____ effect and is seen in ______

ED50 is the dose required for 50% __________ to obtain the ____ effect and is seen in ______

A

individual; max; lab tests

of the population; therapeutic; clinical effects

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52
Q

IC50 is the measure of the _______of a substance in inhibiting a ____________ by 50%

A

potency; specific biological or biochemical function

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53
Q

You want IC50 to be high when you want to see ____ activity whereas you want EC50 to be high when you want to see _____ activity

A

decreased; increased

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54
Q

if Kd is ___ binding affinity is ____

A

low; high

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55
Q

___ is the concentration (molar) of free drug at which 1/2 amt of possible receptors are bound bound

A

Kd

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56
Q

Kd is _______ (directly or inversely) related to binding affinity

A

inversely

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57
Q

EC50 is generally ____ (lower, higher) than Kd

A

lower - b/c some spare receptors

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58
Q

____ is the maximum number of receptors that can be bound

A

Bmax

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59
Q

spare receptors occur when (2)

A
  1. drug dosent bind long but effect lasts (drug bouncing around to diff receptors)
  2. # of available receptors > # of effector molecules `
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60
Q

____ is the median effective dose - at which 50% of individuals exhibit the specific effect

A

ED50

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61
Q

____ is the median lethal dose - at which 50% of individuals exhibit a toxic effect

A

TD50

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62
Q

________ relates dose of a drug required to produce a desired effect to that which produced an undesired effect

A

Theraputic index

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63
Q

Theraputic index equation

A

TI = TD50/ED50

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64
Q

A safe drug has a ____ theraputic index b/c need a _____ dose for toxic effects and a ____ dose to be effective (high, low)

A

high; high; low

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65
Q

What are the 4 kinds of transmembrane receptors and how do they work

A
  1. transmembrane receptor protein - acts as an enzyme intracellular when ligand binds outside
  2. Transmembrane receptor bound to enzymatic protein (tyrosine kinase)
  3. ligand gated ion channel - open or closed w/ ligand binding
  4. Transmembrane receptor protein coupled with G protein - modulates second messenger production inside cell
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66
Q

How do lipid soluble ligands work?

A

cross membrane and act on intracellular receptor = stimulates gene transcription via binding to DNA sequences
ex. steroid hormones

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67
Q

steroid hormone (lipid soluble ligand) effects occur (when) ______ and last for ________

A

lag period (hours-days) ; hours-days

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68
Q

cytokine receptors are an example of ________

A

transmembrane protein receptors with intracellular enzymatic activity or stimulate protein tyrosine kinase

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69
Q

acetylcholine nicotonic receptor is an example of a ____________. Its effects take ________

A

ligand-gated transmembrane ion channel; milliseconds (instant)

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70
Q

the activated alpha unit in the GPCR ________ resulting in ________

A

exhanges bound GDP with GTP; dissociation of alpha subunit from beta-gamma dimer

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71
Q

The 2 signalling cascades of G protein coupled receptors are _____ & _____ and depends on ______

A

cAMP and phosphatidylinositol ; alpha subunit type

72
Q

cAMP mediates
_____ in liver
_____ in kidney
____ homeostasis
______ in heart tissue
_______ of smooth muscles
regulation of __________

A

carb breakdown
water conservation
Ca2+
increased rate of contraction
relaxation
Adrenal and sex steroids

73
Q

Describe the cAMP mechanism (5 steps)

A
  1. GTP activates adenyl cyclase
  2. adenyl cyclase converts ATP –> cAMP
  3. cAMP stimulates cAMP-dependent protein kinases
  4. protein kinases activate/ deactivate further proteins
  5. cascade effect
74
Q

Phosphoinositides (PPIs) are membrane bound _____. They regulate (4 processes in cell)

A

lipids
1. migration
2. proliferation
3. survival
4. diffrentiation

75
Q

phosphatidylinositol is a _____ and mediates the generation of _____ by it’s phosphorylation and dephosphorylation

A

membrane lipid precursor ; PPIs

76
Q

Provide 2 examples of interplay among signalling systems (one opposite, one working together)

A
  1. vasopressor agents contact smooth muscle by phospholipid mediated mobilization of Ca2+ & agents that relax smooth muscle act by elevation of cAMP
  2. in the liver cAMP and phosphoinositide work together to stimulate glucose release
77
Q

almost all 2nd messenger signalling involves ______ phosphorylation.

A

reversible

78
Q

In terms of a signal - phosphorylated = _______ (via _____) dephosphorylation = _________

A

activation (via kinases); terminates effect

79
Q

_____ is the transfer of drug from its site of administration to the blood stream

A

absorption
- IV has none b/c direct into blood stream

80
Q

most drugs are absorped by the manner of ______ transport

A

passive

81
Q

__________ and __________ are important PK parameters

A

fraction of administered dose ; rate of absorption

82
Q

List 5 factors that affect absorption

A
  1. conc. gradient - drugs move from [high] –> [low]
  2. blood flow to absorption site
  3. total surface area available for absorption - bigger = more
  4. contact time with absorption - more time = more
  5. drug properties - lipid solubility, molecular weight, polarity
83
Q

a ______ (charged or uncharged) is hydrophobic and can _______ diffuse across lipid bilayer membranes.

a _____ (charged or uncharged) drug is hydrophilic and cannot diffuse

A

uncharged; passively
charged

84
Q

most drugs are the salts of _____ acids or bases

A

weak

85
Q

relative amounts of protonated and unprotonated forms depends on the drug’s ______ and the environment’s ____

A

pka; pH

86
Q

The two mechanism that drugs can cross a cell membrane include _______ and _________

A

passive diffusion; protein-mediated transport (facilitated or active transport) `

87
Q

________ is the fraction of unchanged drug reaching the systemic circulation following any administration

A

bioavailability

88
Q

______ bioavailability is the amount of drug from a formulation that. reaches the systemic circulation relative to an IV dose

A

absolute

89
Q

______ bioavailability is the amount of drug from a formulation that reaches systemic circulation relative to a different formulation (non-IV)

A

relative
- can compare drugs via ratio at relative

90
Q

___________ for the test and reference formulation/route is used to calculate bioavailability

A

ratio of area under the curve (AUC)

91
Q

For AUC curves _______ is the time in the therapeutic range

A

duration of action

92
Q

For AUC curves __________ is the conc. for therapeutic benefits

A

theraputic range

93
Q

For AUC curves _______ is the time to get in the therapeutic range

A

onset time

94
Q

____ is the max conc of drug found in the body and _____ is the time of Cmax

A

Cmax; Tmax

95
Q

there are different _____ and ______ of AUC for different routes of administration

A

shape and size

96
Q

________ is a phenomenon in which a drug gets metabolized at a specific location in the body -results in reduced conc. of active drug when reaching its site of action or systemic circulation

A

the first pass effect

97
Q

the first pass effect is most toften associated with the _____ but can also occur in ____, ______, _____

A

liver; lungs, vasculature, GI tract (metabolic enzymes)

98
Q

______ is a # you. can use to calculate how much drug you have in your body if you know the conc. of drug in your body

A

Volume of distribution (Vd)

99
Q

the _____ the Vd the more likely the drug is found in the tissues of the body.

the ______ the Vd the more likely the drug is confined to the circulatory system

A

larger; smaller

100
Q

Drugs with Vd:
< /= 4L are ______
4L –> 7L are _____
> 42 are ______

A

< /= 4L are - confined to plasma
4L –> 7L are - distributed throughout blood
> 42 are - distributed to all tissues in body (esp. fatty)

101
Q

_______ is the time required to change the amount of drug in the body by 1/2 during elimination.

A

half life

102
Q

half life is relative to ______ and over time _____

A

Cmax; stays constant ( not dependent on amt of time).

103
Q

_____ is the rate of drug elimination divided by plasma concentration of the drug

A

clearance (CL)
note: elimination means removal of active drug not excreted.

104
Q

The formula for half life is

A

half-life = (0.693 • Vd)/ CL rate
- Vd and CL provided

105
Q

______ is the process by which drug reversibly leaves the blood stream (moving b/w body compartments or reaching target receptors)

A

distribution

106
Q

list 4 factors affecting distribution

A

1.Organ blood flow
- faster if highly perfused = rapid onsett
2. molecular size
- for extremely large - cant get out of blood
3. lipid solubility
- important for the brain and transport mechanisms
4. plasma protein binding
- bound = inactive - depends on affinity

107
Q

_____ is the conversion of a parent (original) drug to metabolite(s)

A

metabolism

108
Q

the goal of metabolism is to make the drug ____ polar to ______ renal excretion

A

more; increase

109
Q

metabolism occurs primarily in the _____ as well as some in the ____, ____, _____, _____

A

liver; gut, lungs, plasma, brain

110
Q

Phase 1 of metabolism involves _____, ______ and _____ reactions with the. majority being _______

A

oxidative, reductive, hydrolytic; oxidative

111
Q

phase 1 of metabolism is catalyzed by _________ isoforms. aka hepatic oxidative isoenzymes

A

cytochrome P450 (CYP)

112
Q

_____ increase enzyme activity = metabolism ______. Cause of many drug-drug interactions that____ potential clinical effects (___ drug)

A

inducers; speed up ; lower; less

113
Q

____ decrease enzyme activity = metabolism _____. See toxic effects b/c you stay in therapeutic range____ and _____ Cmax

A

inhibitors; slows down; longer; increase

114
Q

in phase II of meabolism _______ enzymes which are _____ liver enzymes covalently add ____, _____, _____ molecules to parent drug or phase I metabolite to prep for excretion

A

conjugation; non P50; large, polar, endogenous`

115
Q

List 2 alternative sequences of metabolism

A
  1. some drugs enter phase II directly
  2. some drugs skip metabolism all together
116
Q

______ are administered as an inactive drug that relies on metabolism to produce pharmacologically active produce

A

Produrgs
ex. codeine –> morphine (via CYP2D6)

117
Q

3 pathways of drug excretion in kidney
____ glomular filtration
______ tubular secretion
_______tubular reabsorption

A
  1. Passive glomular filtration - small drugs
  2. Active Tubular secrettioon - large drugs + transport proteins
  3. Passive tubular reabsorption - reabsorbed back into blood –> urine (pH is key)
118
Q

A carrier mediated process. that is not limited by passive diffusion rules excretes larger drugs by secreting them from the _____ to ______ via ________

A

liver; intestine; common bile duct.

119
Q

_____ nerves are craniosacral meaning they originate from the ________ regions of the spinal cord

A

PNS; top and bottom

120
Q

_____ nerves are thoracolumbar meaning they orginate from the ___________ regions fo the spinal cord

A

SNS; thoracic and lumbar

121
Q

SNS ganglia have ____ chains to the ganglia from the spinal cord vs PNS

A

shorter

122
Q

most drugs work at the _________ receptors on ________

A

postganglionic ; target organs

123
Q

Acetylcholine (ACh) is released onto _______receptors at _________ and __________in both PNS and SNS. but only onto _____. receptors in PNS

A

nicotinic; ganglia; target organs; muscarinic

124
Q

ACh is synthesized from ______ and _______ and stored in synaptic vesicles

A

Acetyl CoA and Choline

125
Q

Catecholamines NT such as dopamine, NE and Epi are synthesized from ______

A

tyrosine

126
Q

Nm receptors are found in ______
Nn receptors are found in _____, _____, _____, _____

A

muscle
ganglia, adrenal, CNS, immune

127
Q

PNS receptors are _______ and have __ subtypes . ____ (more or less) drugs target these receptors and they are important for _________

A

muscarinic; 5; fewer; drug side effects

128
Q

_________(number of M receptors) cause _____ bladder muscle contraction via increased ____–>____and are ___ (q or i) G protein coupled

A

M1,M3,M5 ; smooth; PLC –> IP3; Gq

129
Q

_________(number of M receptors) cause _____ heart rate via decreased ___ –> ____ and are ___ (q or i) G protein coupled

A

M2, M4; decreased; AC –> cAMP; Gi

130
Q

The effects of a _____ (PNS) agonist oppose those of an _____ (SNS) agonist

A

muscarinic; adrenergic

131
Q

Effects of a muscarinic agonist in
heart -
lungs-
sphincers (GI and bladder)-
Walls (GI and bladder) -

A

heart
- decreased rate and contraction
lungs
- bronchoconstriction
sphincers (GI and bladder)
- relax (M3)
Walls (GI and bladder)
- contract (M3)

132
Q

In the _____ (PNS or SNS) How does coordinated action lead to urination.

A

PNS
- M3 (bladder wall) = contract
- M3 (sphicter) = relax

133
Q

____ (PNS or SNS) muscarinic receptors _____ secretion (salivary, respiratory, tears)

A

PNS; increase

134
Q

to directly stimulate M receptors you use _______
to indirectly stimulate M receptors you use _______ both which ______ Ach

A

an agonist; acetylcholinesterase (AChE) inhibitors; increase

135
Q

______ (rapid recovery) and _______ (slower recovery) are reversible reaction when cholinesterase is bound (more ACh). Whereas ______ is irreversible

A

Acetylation (rapid- physiological); Cabamylation (slower - drugs); phosphorylation

136
Q

parasympatholytics (aka anticholinergics) block _______ (PNS or SNS) response/ _____receptors. ex. Atropine

A

PNS; muscarinic

137
Q

side effects of anticholinergic drugs (ex. atropine)
mouth -
heart -
gut -
bladder -

A

mouth - dry
heart - tachycardia
gut - constipation
bladder - difficulty urinating

138
Q

_____ receptors in the SNS constrict smooth muscles

A

alpha - 1. (a-1)

139
Q

a-1 receptors constrict ______ in _____ and most critically on _____ for ______

A

sphincters; bladder and GI tract; blood vessels; vasoconstriction

140
Q

a-1 receptors are ________ (receptor type) that produce ___ which results in ______ Ca2+. leading to smooth muscle contraction

A

G-protein coupled; IP3; increased

141
Q

______ receptors in the SNS inhibit presynaptic NE release

A

alpha - 2 (a-2)

142
Q

a-2 ________(agonist or antagonist) would lead to no NE released into synapse

A

agonist

143
Q

_____ receptors in the SNS stimulate the heart rate, AV conduction and contraction.

A

Beta - 1 (B-1)

144
Q

B-1 receptors are ________ (receptor type) that produce ___ which results in ______ Ca2+. leading to increased HR contractility

A

G-protein coupled; AC/cAMP; more channels

145
Q

B-1 receptors in the ____,____, ____. are only innervated by the ____(SNS or PNS)

A

liver, kidney, uterus; SNS

146
Q

B-1 receptors in the kidney _____ renin release which causes a _____ in blood pressure

A

stimulate ; increase

147
Q

_____ receptors in the SNS cause relaxation of smooth muscles

A

Beta-2 (B-2)

148
Q

B-2 receptors cause _____ (dilation or contraction) in the ____, _____, and (contraction or relaxation) in the walls of ____, ____, ____

A

dilation; lungs, blood vessels (skeletal muscle)
relaxation; bladder, uterus, GI tract

149
Q

there is a coordinated effect between _____ and B-2 receptors

A

a-1

150
Q

B-2 receptors are ________ (receptor type) that produce ___ which results in _____

A

G-protein coupled; AC/cAMP; dilation

151
Q

How does coordinated action of SNS receptors lead to peeing

A

bladder wall (B-2) contracts
sphincter (a-1) relaxes

152
Q

B-2 receptors in the ____ mediate glucose release by ______ and ________ which _____ blood glucose conc.

A

liver; gluconeogenesis and glycogenolysis; increases

153
Q

_________ are drugs that mimic sttimulation of the SNS

A

sympathomimetics

154
Q

sympathomimetics work by 2 mechanisms …

A
  1. directly activating adrenergic receptors (NE and Epi)
  2. increasing amt of NE and Epi in synapse
155
Q

what are the three ways sympathomimetics work to. increase the amt of n.t in the synapse?

A
  1. increase n.t release
  2. inhibit reuptake of n.t - inhibit reuptake pumps
  3. inhibit metabolism of n.t - enzymes for catecholamine breakdown
156
Q

__________ are drugs that block or reduce sympathetic activity

A

sympatholytics

157
Q

sympatholytics work by 2 mechanisms..

A
  1. blocking adrenergic recepors (ex. propranolol)
  2. decrease amt of epi and NE released into synapse (ex. clonidine)
158
Q

propranolol is a __________ drug that works by …. and acts on ____ receptors

A

sympatholytic; directly blocking adrenergic receptors; B-1

159
Q

clonidine is a _________. drug that works by … and acts as an. _____ receptor agonist

A

sympatholytic; decreasing the amt of SNS n.t released into the synapse; a-2 agonist

160
Q

What are the 2 different iris muscles and how do they affect the pupil when contracted

A

Circular (sphincter) - contract = constrict pupil
Radial (longitudinal)- contract = dilate pupil

161
Q

Circular (sphincer) contracting resuls from ______(PNS or SNS) stimulation of ____ receptor(s). = ________(constrict or dilate) pupil

A

PNS; M2, M3; constrict

162
Q

Radial (longitudinal) contracting results from______(PNS or SNS) stimulation of ____ receptor(s). = ________(constrict or dilate) pupil

A

SNS; a-1; dilate

163
Q

The most common ways to. treat glaucoma are to increase _____ of AH and decrease______ of AH

A

drainage; production

164
Q

In the PNS ______ receptor(s) stimulation results in ______ ciliary muscle, _____ meshwork and canal = (increased or decreased)_____ drainage

A

M2, M3; contract; open; increased

165
Q

In the SNS, ____ receptors (increase or decrease) ______AH secretion so ______ drugs are used to (increase or decrease) ______ secretion

A

B-2; increase; B-2 antagonists; decrease

166
Q

In SNS, _____ receptors (increase or decrease) ____drainage and ______ production of AH so _____ drugs are used

A

a-2; increase; decrease; a-2 agonists

167
Q

In the PNS side effects of ____ receptor stimulation causes ____ of ciliary muscles = the lens to bulge which improves ____ vision and blurs ___ vision (near or far)

A

M; contraction; near; far

168
Q

List the PNS and SNS receptors found in the GI tract

A

M3 - contract walls, relax sphincters
a-1 - contraction of sphincters
B-2 - relaxation of wall

169
Q

List the PNS and SNS receptors found in the heart

A

M2 - decrease HR and contraction
B-1 - increase HR , AV conduction and contraction

170
Q

List the PNS and SNS receptors found in the blood vessels

A

a-1 - vasoconstriction
B-2 (in skeletal muscle) - vasodilation

171
Q

List the PNS and SNS receptors found in the bladder

A

M3- contraction of walls & relax sphincters
a-1 - contract sphincter

172
Q

List the PNS and SNS receptors found in the bladder

A

M3- contraction of walls & relax sphincters
B-2: relax walls

173
Q

List the PNS and SNS receptors found in the eye

A

M2, M3 - contraction of circular muscles = constrict pupil
a-1 - contraction of radial muscles = dilate pupil

174
Q

List the PNS and SNS receptors found in the kidney

A

B-1 - stimulate renin release = increase BP

175
Q

List the PNS and SNS receptors found in the lungs

A

M: bronchoconstriction
B-2: bronchodilation

176
Q

List the PNS and SNS receptors found in the liver

A

B-2 - increase glucose release via glycogenolysis and. gluconeogenesis

PCTH. 325 (4 decks)

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