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3/ CVS > Cardiovascular Autonomic Pharmacology > Flashcards

Cardiovascular Autonomic Pharmacology Flashcards

1
Q

Describe the organisation of the autonomic nervous system in terms of neurones and neurotransmitters

A

Sympathetics
- Short preganglionic neurone –> ACh –> long postganglionic neurone –> NA
Parasympathetics
- long prehanglionc neurone –> ACh –> short postganglionic neurone –> ACh

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2
Q

What are the 4 cardiovascular effect of sympathetic stimulation?

A
  • increased heart rate and contractility
  • vasoconstriction
  • some vasodilation
  • regulation of renin release for volume control
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3
Q

Which adrenergic receptors are responsible for the following?

  • increased heart rate and contractility
  • vasoconstriction
  • some vasodilation
  • regulation of renin release for volume control
A
  • B1
  • a1, a2
  • B2
  • B1
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4
Q

Where are the perivascular nerves found?

Why do large vessels not respond well to sympathetic activity?

A

In the adventitia of blood vessels

Large vessels don’t respond well as far nerves are far away from target cells

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5
Q

Selective agents with CV relencance:

  1. a1 agonist
  2. a2 agonist
  3. B1 agonist
  4. B2 agonist
A
  1. phenylephrine
  2. clonidine
  3. dobutamine
  4. salbutamol
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6
Q

Selective agents with CV relevance:

  • a1 antagonist
  • B1 antagonist
A
  • dozazosin

- metoprolol

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7
Q

What are the 4 effects of B-adrenoreceptor activation/

A
  • increase heart rate (positive chronotropic effect)
  • increased contractility rate (positive inotropic effect)
  • increased automaticity (tendency to reverse owns electrical rhythm, helpful in asystole
  • fast relaxation and recovery (lusitropic effect)
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8
Q

Intracellular pathways for B-adrenoreceptor activation
Which four channels are upregulate by beta-1 agonist and how?
What two other effects does it have

A

B1 agonist binds, Gs, cAMP, PKA

  • Ca2+ channels - increased Ca2+ entry
  • K+ leak channels for faster repolarisation
  • Na+K+ATPase
  • If (funny current) - positive chronotropy
  • increased ER Ca2+ uptake
  • increase Ca2+ sensitivity
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9
Q

What is the most important agonist clinically?
Where does it act?
What are its uses?

A 
Adrenaline 
B and a adrenoreceptors 
- asystole, VF
- anaphylaxis
- local vasoconstriction e.g with local anaesthetics
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10
Q

Give an example of a B1 agonist

What is used for?

A

Dobutamine

- used to treat carcinogenic shock by providing ‘inotropic support’

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11
Q

What are the classical and alternative pathways for a1 activation in smooth muscle?

A 
Classical pathway
- Gq --> PLC --> PIP2-->  InsP3 mediated Ca2+ release from SR 
Alternative pathways 
- through PKC
- through rho-kinase
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12
Q

Give an example of an a1 agonist
What are its effects?
What is it used to treat/

A

phenylephrine
vasonstriction
used to treat nasal congestion - sudafed

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13
Q

Give an example of an a1 antagonist
What does it do?
What can it treat?

A

Doxazosin

  • causes vasodilation
  • hypertension, Raynaud’s
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14
Q

Give examples of betablockers
What are the actions?
What are they used to treat?

A

propranolol, metoprolol, atenolol

  • negative chronotropic actions
  • negative inotropic actions
  • decrease work done by heart
  • used to treat angina, heart failure, cardiac arrythmias, hypertension
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15
Q

Give an example of a mixed a and B antagonist
What does it do?
What is it used in?

A

carvediol
inhibits a particular cardiac K+ channel (TASK1), leading to class 3 antidysrhythmic action
HEART FAILURE

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16
Q

Why do B-blockers decrease BP?

A
  • decerase CO, esp during exercise/stress - may lead to resting of baroreceptors
  • B1 receptors in kidneys lead to renin release
  • inhibit the tropic effects of catecholamines in the heart (and hence inhibit cardiac hypertrophy with both hypertension and heart failure)
17
Q

What re the cardiovascular effects of parasympathetic stimulation on the heart and blood vessels?

A

Heart
- negative chronotropic effect through action at the SAN
- slow AVN conduction
- little effect on myocardial contractility
Blood vessels
- limited vasodilation, because limited innervation, despite widespread endothelial mAChRs
- complicated by muscarinic receptor-induced release of NO from endothelial cells

18
Q

What are the two main M2-mediated pathways in the heart?

A
  1. Direct G-protein mediated activation of KACh

2. Inhibition of adenylate cyclase - opposing PKA mediated actions on a range of channels

19
Q

What are the cardiac effects of atropine? Where does it act?
What are its other effects?
What is its key use?

A
  • block cardiac M2 receptors
  • decreased secretions. bronchodilation, constripation, urinary retention, pupillary dilation, confusion/hallucinations
  • to treat supra ventricular bradycardia, particularly in the presence of low CO
20
Q

What are the other sympathetic pathways targeted by drugs?

A

storage
uptake of noradrenaline
release of noradrenaline
metabolism in sympathetic neurones

21
Q

Which drug affects storage of NAd?

A

Reserpine:

  • enters sympathetic nerve terminals
  • inhibits NAd transport into vesicles by inhibiting VMAT, depleting of VMAT
  • historically used as an antihypertensive, but depression
22
Q

Which drugs affect reuptake of NAd?

A

cocaine and tricyclic antidepressants e.g. imipramine
block neuronal uptake mediated by NAT (NAd transporter)
causes pro-arrythmetic effects

23
Q

Which drugs affect release of NAD

A

Indirectly acting sympathomimetic amines
e.g. tyramine, ephedinr, amphetamine
Tyramine is found in many foods, which can cause an increase in blood pressure, particularly in conjunction with MAO inhibitors
- cause of reversal of noradrenaline transport through NET, and so cause release

24
Q

Which drugs affect metabolism?

A

MAO

  • blocker are the MAOIs e.g. phenelzineu, iproniazid
  • catchall o-methyltransferase - blocked by entacapone

3/ CVS (19 decks)

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