E1: Powerpoints Flashcards by Jenna Wilkerson

N_M

post-junctional; skeletal neuromuscular junction

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N_N (N_2)

Autonomic ganglia, adrenal medulla

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sympathetic post-ganglionic; some pre-synaptic, lungs

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myocardium, smooth muscle, some pre-synaptic sites, lungs

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lungs, urinary bladder

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M4, M5

No pharmacologic agents

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Predominant tone of the SNS (2 locations/actions)

Arteries: vasoconstriction
Kidney: renin secretion

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Predominant tone of PNS (2)

Detrusor muscle (bladder)
Resting state

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Spinal efferents of SNS

Thoracic and lumbar
Paravertebral ganglion

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Spinal efferents of PNS

Cranial, cervical, sacral (ganglion in organs)
Vagus nerve (cranial nerve X, 75% of all PNS activity)

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What agents are not use clinically but block the uptake of choline

Hemicholinium and vesamicol

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What disrupts SNAPS to prevent the release of Ach into the synaptic cleft

botulinum toxin derivatives

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alpha-1 locations
Alpha-1A locations

arteries smooth muscle
Alpha-1A: prostate, urethra

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beta-1

heart muscle

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beta-2

lung, heart

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beta-3

fat cells, urinary bladder (detrusor)

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what is the rate limiting enzyme of the adrenergic nerve terminal and what does it do

tyrosine hydroxylase, converts Tyr to DOPA

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How does NE get degraded in the synaptic cleft

by COMT

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what influences neurotransmitter release (2)

autoreceptors and heteroreceptors

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where are autoreceptors found and what do they do

alpha2, decrease NE release

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what are heteroreceptors? what NT do they affect

receptors with the ability to influence neurotransmitter release but have less profound effects than autoreceptors
they act on muscarinic receptors to inhibit NE release and on AT1 to stimulate NE release

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Metryrosine-Demser

TH inhibitor (decrease NE synthesis)

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Reserpine

VMAT inhibitor (inhibits NE storage)

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Bretylium

SNAP inhibitor (inhibit NE release)

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Phenylzine-Nardil

MAO inhibitor (increase NE in nerve terminal)

Cocaine

inhibits NET; increase NE in synaptic cleft by inhibiting its reuptake

what type of receptors are at the neuromuscular junction

The ach receptors are only nicotinic (N_M)

phenylephrine is a __________ agonist

alpha-1 agonist

clonidine-Catapres is a ________ agonist

alpha-2 agonist

methyldopa-Aldomet is a ______ agonist

alpha-2 agonist

what agent is a non-selective alpha agonist

oxymetazoline

what agent is a beta-1 agonist

dobutamine-Dobutrex

albuterol-Ventolin is a ______ agonist

beta-2 agonist

mirabegron-Myrbetriq is a _______ agonist

beta-3

what agent is a non-selective beta-1, beta-2 agonist

isoproterenol

what agent is a non-selective adrenergic agonist

epinephrine

what agent is a indirect acting adrenergic agonist that causes the release of NE

pseudoephedrine

what agent is a mixed acting adrenergic agonist so it targets alpha-1, alpha-2, beta-1, beta-2 agonist and causes the release of NE from the nerve terminal

ephedrine

dopamine is a ______ agonist

dopamine (beta-1 and DA-1)

fenoldopam-Corlopam is a _____ agonist

dopamine agonist (beta-1, DA-1)

what agent is used for hypotension/shock (IV)

phenylephrine

what agent's MOA is to selectively bind to alpha-1 adrenergic receptors post-synaptically in effector cells

phenylephrine

what agent's pharmacologic effect is causing vascular smooth muscle receptor stimulation to cause vasoconstriction in blood vessels, arteries throughout the body and vagal afferent induced decrease in HR

phenylephrine (indication is hyPOtension/shock, MOA to bind to alpha-1 adrenergic receptors (located in blood vessels))

what 3 systems does phenylephrine have potential ADR

CV, CNS, endocrine

what are the CV ADR(s) of phenylephrine

Increased BP

what are the CNS ADR(s) of phenylephrine

nervousness, excitability, insomnia

what are the endocrine ADR(s) of phenylephrine

hyperglycemia alpha1 receptors in liver increase glucose production and secretion possible decreased insulin secretion that increases blood glucose

what are the warnings/precautions of phenylephrine

patients w/hypertension, ischemic heart disease, diabetes mellitus

what agent is an alpha-2 adrenergic agonist with a TTS patch available

clonidine (Catapres)

what alpha-2 adrenergic agent is indicated for HTN and ADHD (ER-Kapvay)

clonidine (Catapres)

what alpha-2 adrenergic agent is indicated for HTN in pregnancy

methyldopa (Aldomet)

what is the MOA for clonidine (Catapres)

alpha2a receptor stimulation presynaptically (autoreceptor)/ post-synaptically (CNS) decreasing sympathetic tone overall decrease in sympathetic impulses in CNS

what 3 things does the presence of phenols/catechols on a benzene ring do

1: decrease lipophilicity 2: decrease CNS penetration 3: more likely to be metabolized by COMT

Which confers to beta-2 receptor selectivity? 3,4 or 3,5 dihydroxy

3,5

If you substitute/replace the OH on the ring _______ _______ receptor selectivity

increase Beta-2

Substitution on ____ carbon blocks oxidation by MAO and prolongs duration of action

alpha

what type of compounds are more likely to cause release of NE from storage since they stay in the nerve terminals longer

alpha-methyl compounds

what group does Clonidine have on its structure that increases its CNS penetration

halogens which increase lipophilicity

Catapres is 300x more active on _____ than ____

more active on alpha 2 than alpha 1

substitution on ____ carbon increases activity at both alpha and beta adrenergic receptors

beta

hydroxyl groups decrease actions within the CNS therefore decreasing lipid solubility when there are substitutions on ___ _______

beta carbon

If there is a methyl substitution on the amine the compound reacts with which receptors Give an example

alpha-1, beta-1, beta-2 Epinephrine, the small methyl groups allows it to retain the alpha1 receptor affinity

If there is an isopropyl, t-butyl, or other bulky group substitution on the amine, the compound will react with

beta1 and beta2 if isopropyl group only beta2 if t-Bu or larger (double activity)

Loss of ____ binding increases with nitrogen substitution

alpha

what is the order of increasing potency in which catecholamines stimulate beta-adrenoreceptors

norepinephrine < epinephrine < isoproterenol

MAO metabolism occurs at _____

amines

_____ are more susceptible to MAO metabolism, why

primary amines; large substitution decreases MAO metabolism

where does COMT metabolism occur on a structure

OH on a benzene ring

which metabolism takes place orally resulting in rapid inactivation in intestine and liver

COMT metabolism

what are the 4 criteria for high agonist activity

1) primary or secondary amine 2) amine separated by 2 carbons from benzene ring (ethyl) 3) hydroxyl group on B carbon 4) 3,4 di-OH for alpha and beta receptor activity