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Physiology > Cardiovascular Autonomic Pharmacology (B2: W3) > Flashcards

Cardiovascular Autonomic Pharmacology (B2: W3) Flashcards

1
Q

What is the efect of cAMP on smooth muscle contraction?

A

Inhibition of contraction

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2
Q

Where are alpha 1 receptors located and what is their mechanism of action?

A
  • Smooth muscle: blood vessels, eye, gut, bladder sphincter
  • Formation of IP3 and DAG (PKC)
  • Contraction
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3
Q

Where are alpha 2 receptors located and what is their mechanism of action?

A
  • Presynaptic nerve terminals, some vascular smooth muscle
  • Inhibition of neuronal Ca channels, inhibition of adenylyl cyclase
  • Constriction
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4
Q

Where are ß1 receptors located and what is their mechanism of action?

A
  • Cardiac myocytes, juxtaglomerular cells
  • Stimulation of adenylyl cyclase, increased cAMP
  • Response:
    • Heart: increasing rate (SA), conduction velocity (AV), contractility rate of relaxation
    • Kidney: increase renin secretion
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5
Q

Where are ß2 receptors located and what is their mechanism of action?

A
  • Smooth muscle (airways, blood vessels), ciliary body epithelium, cardiac muscle
  • Stimulation of adenylyl cyclase, increased cAMP
  • Response:
    • Heart: increase heart rate and contractility
    • Smooth muscle: relaxation
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6
Q

What are the autonomic effects on the SA node?

A
  • Sympathetic activation of ß1 receptors has a positive chronotropic effect (increases HR)
  • Parasympathetic activation of M2 muscarinic receptors has a negative chronotropic effect (decreases HR)
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7
Q

What are the autonomic effects on the AV node?

A
  • Sympathetic activation of ß1 receptors has positive dromotropic effect (increases conduction velocity)
  • Parasympathetic activation of M2 receptors has a negative dromotropic effect (decreases HR)
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8
Q

What are the autonomic effects on the ventricular muscle?

A
  • Sympathetic activation of ß1 receptors has a positive inotropic effect (increases contractility)
  • Parasympathetic activation of M2 receptors antagonizes sympathetic responses
    • In the absence of sympathetic tone, parasympathetic activation has little or no effect on the ventricles
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9
Q

What effect does sympathetic ANS stimulation have on blood vessels

A
  • Alpha 1 receptors cause vascular smooth muscle contraction and constriction of the blood vessels
  • ß2 receptors cause relaxation of vascular smooth muscle and dilation of blood vessels
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10
Q

What effect does parasympathetic ANS activation have on blood vessels?

A
  • Parasympathetic activation has little or no effect on most blood vessels
  • Exceptions: blood vessels of the face, tongue, genitals, and urinary tract, where parasympathetic stimulation causes vasodilation
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11
Q

What is the receptor sensitivity to Norepinephrine?

A

ß1 = a1 ≥ a2 > ß2

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12
Q

What is the cardiovascular response to Norepinephrine?

A
  • Increase in diastolic, systolic, and mean arterial pressure
  • Decrease in heart rate
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13
Q

Why does heart rate decrease with norepinephrine?

A
  • a1 receptor activitiy causes increase in mean arterial pressur (MAP)
  • Baroreceptors sense this reflex, and try to bring it back with an increase in parasympatheti tone
    • Decrease HR
  • Fast response
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14
Q

What is the receptor selectivity to epinephrine?

A

ß1 = ß2 > a1 = a2

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15
Q

What is the cardiovascular response to epinephrine?

A
  • Increased heart rate
  • Increased systolic BP, decreased diastolic, MAP stays the same
  • Decreased peripheral resistance
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16
Q

Why does peripheral resistance decrease in response to epinephrine?

A
  • At low doses, ß2 receptors cause vasodilation
    • Decreased diastolic BP
    • Similar response to isoproterenol
  • At higher doeses, the a1 vasoconstriction can be seen
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17
Q

What is the receptor selectivity of isoproterenol?

A

ß1 = ß2

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18
Q

What is the cardiovascular response to isoproterenol?

A
  • Increased heart rate
  • Increased systolic, decreased diastolic, slight decrease in MAP
    • ß2 - peripheral vasodilation
  • Large decrease in peripheral resistance
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19
Q

Why is there a larger decrease in peripheral resistance with isoproterenol than epinephrine?

A

Epinephrine still has some a1 selectivity, as where isoproterenol has none

  • Epineprhine has some vasoconstriction
  • Isoproterenol has very little
20
Q

What happens to the cardiovascular response to epinephrine at higher doses?

A
  • Higher diastolic pressure and MAP
    • More a1 receptors are activated
    • Increase in TPR
  • Heart rate increased
    • ß1
21
Q

Why does HR still increase at higher doses of epinephrine, but not with norepinephrine?

A

In epinephrine, the ß1 response is stronger than a1

In norepinephrine, the responses are equal, and thus the baroreceptors still modulate to keep the BP down

22
Q

What is the receptor selectivity of dobutamine?

A

ß1 > ß2 > a1

23
Q

What is the receptor selectivity of dopamine?

A

D1 > ß1 = ß2 > a1

24
Q

What is the receptor selectivity of phenylephrine?

A

a1 > a2

25
Q

What is the receptor selectivity of clonidine?

A

a2 > a1

26
Q

What is pulse pressure?

A

Difference between systolic and diastolic pressures

27
Q

What are the dose dependent effects of dopamine?

A
  • Low doses: activate D1 receptors, increasing renal blood flow
  • Intermediate doses: activate ß recetpors, increasing cardiac output
  • High doses: activate alpha receptors, increasing TPR and MAP
28
Q

What is the first line of treatment for hypovolemic shock?

A

Volume replacement

29
Q

What is the first line of treatment in vasodilatory shock (sepsis, anaphylaxis), where cardiac output is reduced?

A

Use a vasoconstrictor - norepinephrine

Epinephrine to increase HR

30
Q

What is the first line of treatment in cardiogenic shock (heart failure), where there is decreased cardiac output with increased venous pressure?

A

Use a ß compount to increas HR and function

Isoproterenol, dobutamine, dopamine

31
Q

What is the effect of clonadine?

A
  • a2 > a1
  • Activates presynaptic a2 receptors, inhibiting sympathetic neruotransmitter release
  • Decreases sympathetic (arterial) tone
32
Q

What is tyramine and what is its mechanism of action?

A
  • Indirect sympathomimetic found in food (cheese, meats, beer)
  • Taken up into postganglionic sympathetic nerve terminals by the norepinephrine transporter (NET)
    • Metabolized by MAO (monoamine oxidase)
33
Q

What happens to tyramine in patients taking an MAO inhibitor?

A

Unmetabolized tyramine can displace endogenous neurotransmitters, causing spontaneous release resulting in a hypertensive crisis

34
Q

What are sympatholytics?

A

Selective blockers of sympathetic effects

35
Q

What is phentolamine and what is it used for therapeutically?

A
  • Sympatholytic: a1 = a2 antagonist
  • Used to treat hypertension and pheochromocytoma
36
Q

What is prazosin and what is it used for therapeutically?

A
  • Sympatholytic: a1 >> a2 antagonist
  • Used to treat hypertension
37
Q

What is propranolol and what is it used for therapeutically?

A
  • Sympatholytic: **ß1 = ß2 **antagonist
  • Used to treat angina, cardiac arrhythmias, hypertension
38
Q

What is metropolol and what is it used for therapeutically?

A
  • Sympatholytic: ß1 > ß2 antagonist
  • Used to treat heart failure, angina, hypertension
39
Q

What is carvedilol and what is it used for therapeutically?

A
  • Sympatholytic: a1 > ß1 > ß2 antagonist
  • Used to treat heart failure, hypertension
40
Q

What is the effect of a beta blockade on epinephrine?

A

Enhances alpha adrenergic response to high dose epinephrine

Large difference in diastolic pressure

41
Q

How do ß1 antagonists reduce blood pressure?

A

Inhibit renin secretion from the kidneys

or

Decrease HR ans stroke volme

(MAP = HR x SV x TPR)

42
Q

What receptor does bethanechol act upon?

A

Muscarinic

43
Q

What receptors are activated by acetylcholine?

A

NM = NN = M1-5

Equally selective

44
Q

What does digoxin (a cholinomimetic) do?

A
  • Can act centrally to increase parasympathetic tone to the heart
    • Goes to CNS first
  • Slows conduction through the AV node
45
Q

What is atropine and what is it used for therapeutically?

A
  • Cholinolytic: M1-5 >> NN = NM antagonist
  • Blocks parasympathetic function
  • Used to treat bradycardia and heart block

Physiology (29 decks)

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