Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key


Play button


Play button




Click to flip

55 Cards in this Set

  • Front
  • Back
SNS regulates these 2 major things. Especially in response to what? What mediates the SNS stimulation?
Heart & Peripheral Vasculature


NE (& Epi from adrenal medulla)
Drugs that mimic the actions of Epi or NE are called what?
Sympathomimetic drugs
List 3 modes of action of Indirecting acting Adrenoceptor-activating agents
1. promote release of Endogenous Catecholamines

2. displace stored catecholamines = Amphetamine & Tyramine

3. inhibit reuptake of Catecholamines (Cocaine)
What is the function of Alpha-1 Adrenoceptors?
Contraction of Smooth Muscle
-Peripheral Vasculature = increase BP
-GI & Bladder sphincters = urinary retention
-radial muscle of iris = mydriasis
-Kidney = decrease Renin release
What is the mechanism of action of the Alpha-1 adrenoceptors?
Activation of Gq
1. stimulate PIP2 hydrolysis
2. formation of IP3 -> Ca++ mobilization
3. formation of DAG -> PKC activation
4. Phospholipase C activation
What is the function of the Alpha-2 adrenoceptors?

What is the mechanism of action?
Presynaptic autoregulation of neurotransmitter release

1. activate Gi
2. inhibition of Adenylyl Cyclase
3. decrease in cAMP

**MAD 2's
Define the affinity of Beta-1 adrenoceptors for Epi & NE

Define the affinity of Beta-2 adrenoceptors for Epi & NE
Beta-1 --> Epi = NE

Beta-2 --> Epi > NE
Where are Beta-1 receptors located?

What is their mechanism of action?
SA node, AV node, and Ventricular muscle of the heart

1. activate Gs
2. stimulate Adenylyl Cyclase
3. increase cAMP levels
Where are the Beta-2 adrenoceptors located?

What is their mechanism of action?
VENOUS vascular smooth muscle, bronchial smooth muscle, and in walls of GI tract & bladder

1. activate Gs
2. stimulate AC = increase cAMP levels
Whare are Dopamine receptors located? (3)
1. Brain
2. Splanchnic vasculature
3. Renal vasculature
What is the difference b/w D1 and D2 adrenoceptors?
D1 = stimulates AC (Gs)

D2 = inhibits AC (Gi)
What is the parent compound of the Catecholamines? Substitutions at what positions yields different catecholamines?
Phenyl-ethyl-amine = benzene ring with ethylamine side chain

positions 3 & 4
Adrenoceptors & Blood Vessels:
1. receptors present on the ARTERIAL smooth muscle = vasoconstriction
2. receptors present on the VENOUS smooth muscle = capacitance
3. receptors on the Skeletal muscle vessels
4. receptors that stimulate Renin secretion
5. receptors that inhibit Renin secretion
1. Alpha-1

2. Beta-2 = relax smooth muscle

3. Beta-2 = relax smooth muscle & allow blood to flow into muscles

4. Beta-1

5. Alpha-1
Adrenoceptor that is dominant in the Heart

What is the function?

results in increased Ca++ influx in cardiac cells = positive inotrophy (faster) & chronotrophy (harder)
-AV conduction velocity increased
-refractory period decreased

**with normal reflexes, HR is dominated by Vagal tone (Muscarinic)!!! = trumps sympathetic
What effect do Alpha agonists have on the Eye?
contract Radial Pupillary Dilator muscle = Mydriasis = excessive dilation of pupil
What effects do Beta agonists have on the Eye?
Increase Aqueous Humor secretion from the Ciliary Epithelium

**Beta-antagonists are important in the treatment of Glaucoma
Respiratory Tract
1. What are the effects of Beta-2 receptors?

2. What are the effects of Alpha-1 receptors?
1. Bronchodilation

2. present in blood vessels of upper respiratory musoca = contraction produces DECONGESTION
GI tract:

1. what are the effects of Beta receptors?

2. Alpha-2 activation effect?
1. present on smooth muscle cells = mediate relaxation

2. decreases PNS drive on enteric system ***major effect***
What adrenoceptors are present in the GU tract? What are their functions?
Alpha-1 = contract bladder base, urethral sphincter = urinary retention

Beta-2 = relax smooth muscle in the bladder wall = promotes urinary retention
What adrenoceptors are present on the Exocrine glands? What is the function?
Alpha-1 on Apocrine (stress) sweat glands

Sweating on palms, brow, upper lip
List the effects Beta-adrenoceptor activation has on metabolism
1. increases Lipolysis
2. enhances Glycogenolysis
3. increases Glucose release
4. increases Insulin secretion (in response to high serum glucose)
What adrenoceptor decreases Insulin release?
Is Insulin increased or decreased during SNS discharge? Why?
Increased due to high serum glucose levels
Endogenous catecholamine that has relatively little effect on Beta-2 adrenoceptors
Norepinephrine = does not cause Venodilation

**but has similar potency to Epi at Beta-1
What are the major effects of Epi release?
Potent vasoconstriction (alpha-1) and Cardiac stimulant (beta-1)
Explain the differences in the effects of Epi & NE
-potent vasoconstrictor (alpha-1) & cardiac stimulant (beta-1)
-Venodilation due to Beta-2 = venous capacitance

-little effect on Beta-2 = no venous capacitance
-increases BOTH diastolic and systolic BP
-peripheral vagal reflexes overcome direct positive chronotrophy
Positive nonselective Beta-receptor agonist (Beta-1 = Beta-2)

What are its effects?

Beta-1 = increase HR, contractility
Beta-2 = decrease diastolic & mean arterial pressures (venodilation)
What effects does Dopamine have?
activates D1 receptors in Renal Vasculature ➡ increases renal blood flow
Relatively Beta-1 selective synthetic catecholamine that also activates Alpha-1 receptors (Beta-1 > Beta-2)

What is it useful for?

Cardiovascular insufficiency
-big increase in resistance = due to Alpha-1 that is unopposed by Beta-2
-Unopposed resistance causes increased Blood Pressure = increased in both Diastolic and Systolic pressures; MAP also increases
-Increased MAP ➡ Vagal response ➡ decreased HR due to PSNS activation of muscarinic receptors
What catecholamine would cause this? Explain
-Alpha-1 = Arterial constriction
-Beta-2 = venous dilation
-MAP doesn’t change
-Widening of Pulse pressure due to Arterial constriction & venodilation
-Beta-1 causes increased HR

**Epi stimulates all Alpha's & Beta's
What would produce this response?
Isoproterenol = selective Beta-agonist (Beta-1 = Beta-2)
-Beta-1 = increased HR
-Beta-2 = venodilation = decreased peripheral resistance
-Systolic goes slightly up due to increased HR & CO from Beta-1
-since MAP is not changed much ➡ no reflex
What would cause this effect? Explain
Prototypic Alpha-1 agonist

What is another alpha-1 agonist?

Why does Phenylephrine have a longer duration of action than the Catecholamines?
It is not a catechol derivative = not inactivated by MAO or COMT
What is Phenylephrine used clinically for?
Alpha-1 agonist
1. Mydriatic = pupil dilator
2. Decongestant

**can also raise blood pressure if used at high levels
Fisrt orally active Sympathomimetic drug

What activity does it have?

Alpha agonist, displaces NE from vesicles (major effect)
Widely available OTC decongestant

What is it's MOA?

Direct alpha adrenoceptor activation & indirect effects causing release of endogenous NE
2 direct Alpha-1 agonists that are used as topical decongestants (nasal spray)

List 4 Alpha-2 selective agonists

What are they used as?

Anti-hypertensives b/c inhibit release of endogenous NE
List 2 Beta-1 selective agonists
What do they do?
Pre-nalt-erol (partial agonist)

Increase Cardiac Output with less reflex tachycardia
-don't cause the Beta-2 stimulated venodilation
List 4 Beta-2 selective Agonists

What are they used to treat?

Uterine relaxation in premature labor (Ritodrine)
Beta-2 selective agonist used for uterine relaxation in premature labor (prevent premature labor)
Indirect sympathomimetic that enters presynaptic neuron via Uptake 1 and releases stores of catecholamines
-marked stimulant effects on mood and alertness
-depressant effect on appetite
-commonly abused drug
What is the difference between Amphetamine and Methamphetamine
Methamphetamine has a higher ratio of central to peripheral actions
Amphetamine variant used in ADHD due to less stimulant effects
What is the mechanism of action of Cocaine?
Sympathomimetic that blocks Uptake 1
1. mechanism of action
2. where is it found?
3. what potentiates its effects?
4. what can it produce?
1. gets in via uptake 1 ➡ has high affinity for VMAT ➡ shoved into vesicles ➡ pushes NE out
2. Fermented foods (cheese) and aged foods
3. MAO inhibitors
4. Hypertensive crisis
In what conditions would Sympathomimetics be used to increased blood flow or pressure?
1. Hypotension (secondary to Cardiac Arrhythmias, neurologic disease)
2. Hypovolemic or Cardiogenic shock
3. Cardiac insufficiency
What would be used to cause Hemostasis for Surgery?
Cocaine = causes vasoconstriction
What would be used to reduce diffusion of Local Anesthetics?
What sympathomimetics would be used to reduce mucous membrane congestion?
Alpha-1 agonists
What might be used to treat Heart Failure?
Dobutamine (Beta-1 agonist)

**but tolerance/desensitization limits used
What sympathomimetic would be used for Fundoscopic examination of the retina?
What sympathomimetic would be used to treat Narcolepsy (daytime sleepiness)?
Amphetamines produce alertness and defer sleep
What would be the symptoms of toxicity of Sympathomimetic drugs?
1. Hypertension

2. Tachycardia

3. CNS