Adrenergic Agonists & Antagonists

Question 1

From where is norepinephrine released?

Answer 1

post-ganglionic sympathetic fibers at end organ tissues (except in eccrine sweat glands and some blood vessels)

Question 2

From where is acetylcholine released?

Answer 2

Preganglionic sympathetic fibers and all parasympathetic fibers

Question 3

How is the action of NorEpi terminated

Answer 3

Primarily reuptakeinto postganglionic nerve ending; also diffusion from receptor sites or via metabolism by monoamine oxidase

Question 4

Where are alpha1-receptors located

Answer 4

smooth muscle throughout the body

Question 5

What is occurs with activation of alpha1-receptors

Answer 5

contraction of smooth muscle

• midriasis, bronchoconstriction, vasoconstriction, uterine contraction, constriction of sphincters
• myocardium has alpha1-receptors –> positive inotropic effect
• most important clinical effect is vasoconstriction

Question 6

What occurs with activation of peripheral alpha2-receptors

Answer 6

Inhibits NorEpi release

Vasoconstriction

Question 7

What occurs with activation of CNS alpha2-receptors

Answer 7

Sedation and reduced sympathetic outflow –peripheral vasodilation and lower BP

Question 8

Where are most B1 receptors located and what occurs with activation of these receptors?

Answer 8

Heart
+ Chronotropy
+ Dromotropy (conduction)
+ inotropiy

Question 9

What occurs with activation of B2 receptors?

Answer 9

Smooth muscle relaxation: bronchodilation, vasodilation, uterus relaxation, bladder and gut

Question 10

What occurs with activation of dopamine receptors - D1 and D2?

Answer 10

D1: mediates vasodilation in kidney, intestine and heart
D2: antiemetic properties (e.g., as in droperidol)

Question 11

What are the naturally occurring cathecolamines and what is unique about their structure

Answer 11

Epinephrine, Norepi, Dopamine

All have a 3,4-dihydroxybenzene structure

Question 12

What receptors does phenylephrine act on and what is its primary effect?

Answer 12

Selective alpha1-agonist

Peripheral vasoconstriction

Question 13

Why does phenylephrine cause bradycardia?

Answer 13

Reflex bradycardia is mediated by the vagus nerve and can reduce cardiac output

Question 14

Can tachyphylaxis occur with phenylephrine infusions? what is a typical infusion rate (mcg/kg/min)?

Answer 14

YES

0.25-1mcg/kg/min

Question 15

What receptors does dexmedetomidine act on?

Answer 15

alpha-2 (200:1 alpha2:alpha1)

Question 16

What is the half life of dexmedetomidine?

Answer 16

2-3 hours

Question 17

What is the recommended dose of dexmed?

Answer 17

loading dose 1mcg/kg over 10 minutes, followed by infusion 0.2-0.7mcg/kg/hour

Question 18

What can occur with abrupt cessation of dexmed after >48h of adminstration?

Answer 18

Withdrawal: hypertensive crisis

Question 19

Where is epinephrine synthesized

Answer 19

Adrenal medulla

Question 20

What is a typical range for an epinephrine infusion?

Answer 20

2-20mcg/min

Question 21

On which receptors does NorEpi act?

Answer 21

Alpha-1 and 2; Beta-1

Question 22

What receptors does dopamine act on at low doses (0.5-3mcg/kg/min)? What effect does this have?

Answer 22

Dopamine receptors (DA1)
Vasodilates renal vasculature and promotes diuresis and natruiresis
No beneficial effect on renal function

Question 23

What receptors does dopamine act on at moderate doses (3-10mcg/kg/min)? What effect does this have?

Answer 23

Beta-1
Increased myocardial contractility, rate, SBP, CO
Myocardial oxygen demand increases disproportionately to supply

Question 24

What receipts does dopamine act on at high doses (10-20 mcg/kg/min):? what effect does this have?

Answer 24

Alpha-1

increase in peripheral vascular resistance (fall in renal blood flow)

Question 25

What is isoproterenol’s mechanism of action?

Answer 25

Beta agonist (Beta 1 and 2)

Question 26

What receptors does dobutamine act on? What are its clinical effects?

Answer 26

B1 and B2 (more selective for B1)
Rise in CO secondary to increased myocardial contractility
Decrease in peripheral vascular resistance (B2 activation)
LV filling pressure decreases
Coronary blood flow increases

Question 27

What is a typical range for dobutamine infusion?

Answer 27

2.5-20 mcg/kg/min

Question 28

How does phentolamine work? What physiological effects are seen?

Answer 28

Alpha-1 and alpha-2 blockade. Causes smooth muscle relaxation and thus lowers BP
This drop in BP leads to a reflex tachycardia

Question 29

What clinical conditions is phentolamine used for?

Answer 29

HTN caused by excessive alpha-stimulation: pheochromocytoma, clonidine withdrawal
Prevention of tissue necrosis following extravasation of IV fluids with alpha agonist (e.g., norepi)

Question 30

What receptors does labetalol act on?

Answer 30

alpha1, beta1, beta2. Alpha to Beta ratio is 1:7

Question 31

How long does it take for Labetalol’s peak effect?

Answer 31

5 minutes (IV)

Question 32

Which beta blockers are selective for Beta1 receptors?

Answer 32

Atenolol, esmolol, metoprolol

Question 33

What is the distribution half life and elimination half life of esmolol? How is esmolol eliminated?

Answer 33

Distribution: 2 minutes
Elimination: 9 minutes
Eliminated by hydrolysis by RBC esterase

Question 34

What is propranolol’s mechanism of action

Answer 34

Non-selective B1 and B2 blocker
Decreases BP by decreasing myocardial contractility, lowering HT, decreasing renin release
Decreases myocardial oxygen demand

Question 35

What is carvedilol’s mechanism of action?

Answer 35

Mixed beta and alpha-blocker

Question 36

Why should alpha-1 receptors be blocked with an alpha antagonist (e.g., phentolamine, phenoxybenzamine) before administration of a beta-antagonist?

Answer 36

Unopposed alpha can lead to extreme HTN