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cvs > cardiovascular autonomic pharmacology > Flashcards

cardiovascular autonomic pharmacology Flashcards

1
Q

Where are beta-1 adrenoceptors located?

A

heart

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2
Q

where are beta-2 adrenoceptors located?

A

blood vessels and heart

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3
Q

in what layer of the blood vessel wall are autonomic nerve endings located?

A

tunica adventitia

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4
Q

where are alpha-1 adrenoceptors located?

A

smooth muscle - blood vessels

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5
Q

where are alpha-2 adrenoceptors located?

A

smooth muscle- blood vessels

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6
Q

what effects does beta-adrenoceptor activation have on the heart?(4)

A
  • increased HR (positive chronotropy)
  • increased contractility rate (positive inotropy)
  • increased conduction velocity (positive dromotropy)
  • faster relaxation and recovery (positive lusitropy)
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7
Q

name 5 beta-agonists

A
  • isoprenaline
  • adrenaline
  • noradrenaline
  • dobutamine (beta-1)
  • salbutamol (beta-2)
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8
Q

describe the intracellular pathway of beta-adrenoceptor activation

A
  • agonist binds to receptor
  • stimulates G-stimulatory protein (GPCR)
  • increase production of cAMP from ATP through adenyl cyclase
  • works through PKA pathway
  • initiate effects in cardiac and smooth muscle
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9
Q

How do beta-1 (primarily) and beta-2 adrenoceptors stimulate increased chonotropy, inotropy, etc. in the heart? (4)

A
  • intracellular pathway (PKA) described before
  • cAMP-dependent protein kinase A phosphorylates L-type calcium channels in cardiac myocytes leading to increased Ca2+ influx > increased Ca2+ release from sarcoplasmic reticulum > increased inotropy
  • activated G-stimulatory protein opens/influences ion channels for ions involved in generating pacemaker currents (Na+ channels - ‘funny current’, K+ channels, Na+/K+ ATPase) thereby increasing chronotropy (HR)
  • PKA phosphorylates sites on sarcoplasmic reticulum > stimulates ryanodine receptors > more release of Ca2+ from SR > more Ca2+ binding to troponin C > increase inotropy
  • PKA phosphorylates myosin light chains >inotropic effect
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10
Q

What effect does beta-2 adrenoceptor activation have on blood vessels and how does this occur?

A

-vasodilation

-agonist binds to receptor
-activates G-stimulatory protein (GPCR)
-stimulates production of cAMP from ATP through AC
-cAMP in smooth muscle INHIBITS myosin light chain kinase (MLCK)
-MLCK phosphorylates myosin
-therefore less contractile force produced in smooth muscle in presence of cAMP
>relaxation of smooth muscle

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11
Q

What effect does beta-2 receptor stimulation in the lungs have?

A

bronchodilation

*remember salbutamol is a beta-2 agonist and is used in inhalers to open up airways!

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12
Q

What effect does beta-2 receptor stimulation in the liver have?

A

hepatic glyogenolysis > increased blood-glucose

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13
Q

What effect does beta-2 receptor stimulation in the pancreas have?

A

release of glucagon > increased blood glucose

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14
Q

What effect does beta-1 receptor stimulation in the kidney have?

A

-leads to renin release
>production of angiotensin II
>vasoconstriction and fluid retention

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15
Q

How do alpha-1 adrenoceptors affect vascular smooth muscle? describe the intracellular pathway(s) for this effect.

A

-vasoconstriction (effect more prominent in arterial vessels)

-agonist binds to alpha-1 receptor
-stimulates Gq protein
-activates IP3-mediated pathway
-increased release of Ca2+ from sarcoplasmic reticulum
-more binding of Ca2+ to troponin C
>increased vascular smooth muscle contraction

  • alternative pathways:
  • through PKC
  • through Rho-kinase
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16
Q

How do alpha-2 adrenoceptors affect vascular smooth muscle? describe the intracellular pathway for this effect.

A

-vasoconstriction (effect more prominent in arterial vessels)

-agonist binds to alpha-2 receptor
-stimulates G-inhibitory protein
-inhibits production of cAMP from ATP by AC
-less inhibition of myosin light chain kinase
>increased vascular smooth muscle contraction

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17
Q

during exercise, sympathetic activity (noradrenaline) increases to blood vessels in skeletal muscle (and other vessels!). SNA affects both alpha-1 and beta-2 receptors but which one predominates? what effect does this cause on vascular smooth muscle?

A

-SNA predominately affects alpha-1 receptors in skeletal muscle
>vasoconstriction

*remember can still get a little vasodilation through SNA

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18
Q

during exercise, circulating adrenaline increases to blood vessels in skeletal muscle (and other vessels!). adrenaline affects both alpha-1 and beta-2 receptors but which one predominates? what effect does this cause on vascular smooth muscle?

A

-adrenaline predominately affects beta-2 receptors in skeletal muscle
>vasodilation

*remember can still get a little vasoconstriction through adrenaline

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19
Q

which cardiovascular receptors does adrenaline target? is it an agonist or antagonist to these receptors?

A

both alpha and beta receptor AGONIST

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20
Q

When is adrenaline prescribed as treatment? (4)

A
  • asystole
  • ventricular fibrillation and other severe arrhythmias
  • anaphylaxis
  • local vasoconstrictor so used in local anaesthetic mixtures
21
Q

What is dobutamine?

A

beta-1 agonist

22
Q

When is dobutamine prescribed?

A

cardiogenic shock (inotropic support)

23
Q

what is phenylephrine?

A

alpha-1 agonist

24
Q

when is phenylephrine prescribed?

A

nasal congestion

25
Q

what is doxazosin?

A

alpha-1 antagonist

26
Q

when is doxazosin prescribed?

A
  • hypertension

- Raynaud’s syndrome

27
Q

give examples of beta-blockers

A
  • propanolol (1+2)
  • metoprolol (1)
  • atenolol (1)
28
Q

when are beta-blockers prescribed?

A
  • angina
  • heart failure
  • cardia arrhythmias
  • hypertension
29
Q

what is carvedilol?

A

mixed beta and alpha antagonist

30
Q

when is carvedilol prescribed?

A

heart failure

31
Q

what is clonidine?

A

alpha-2 agonist

32
Q

why do beta-blockers decrease BP? (3)

A
  • decrease CO esp. during exercise
  • renin release in kidney > RAAS
  • inhibit trophic effects of A/NA in heart (inhibit cardiac hypertrophy associated with hypertension)
33
Q

what effects do parasympathetic stimulation have on the heart? (3)

A
  • decreased chronotropy through action on SA node
  • slows AV node conduction
  • little effect on myocardial contractility
34
Q

do blood vessels have parasympathetic innervation?

A

LIMITED vessels have parasympathetic innervation:

  • genitalia erectile tissue
  • salivary glands
  • GIT glands
35
Q

what effect does parasympathetic stimulation have on vessels (if any)?

A

vasodilation

36
Q

Describe the parasympathetic intracellular signalling pathways of the heart.

A

-ACh released from post-ganglionic vagal neurones innervating the heart
-ACh binds to M2 (muscarinic) receptors mainly found in SA and AV nodes.
-stimulates G-inhibitory protein (GPCR)
>decreases cAMP production from ATP through AC
>decreased inotropy and chronotropy

-also Gi protein activation leads to activation of particular K+ channels
>increase K+ efflux
>cell hyperpolarization
>decreased chronotropy

37
Q

what is atropine?

A

muscarininc antagonist

38
Q

What effects does atropine produce in the heart and throughout the body?

A
  • blocks cardiac M2 receptors

rest of body:

  • decreased secretions (mouth, gut, airways)
  • bronchodilation
  • constipation
  • urinary retension
  • pupillary dilation
  • confusion/hallucinations
39
Q

when is atropine prescribed? (cardiac conditions)

A

supraventricular bradycardia, particularly in low CO

40
Q

Describe the synthesis, release and recycling of noradrenaline in the axon nerve terminal.

A
  • tyrosine transported into sympathetic post-ganglionic axon
  • tyrosine converted into DOPA
  • DOPA is converted into dopamine
  • dopamine is converted into noradrenaline and transported into vesicles by vesicular monoamine transporter (VMAT)
  • an action potential travels down axon, depolarising the membrane
  • causes an influx of Ca2+
  • leads to exocytosis of noradrenaline through vesicles
  • noradrenaline cross synaptic gap to bind to receptors on effector organ
  • 90% of noradrenaline recycled by transport back into nerve terminal
  • this is done by noradrenaline transporter (NAT) and the process is called Uptake 1
  • some noradrenaline taken up by post junctional tissue and metabolised
  • some noradrenaline diffuses into capillaries and is transported in circulation
  • some noradrenaline is metabolised in extracellular space and then diffuses into capillaries
  • non-neuronal uptake of noradrenaline is termed Uptake 2
41
Q

how does the drug reserpine work?

A

enters sympathetic nerve terminals and inhibits VMAT > inhibits noradrenaline transport into vesicles

42
Q

which drugs can inhibit Uptake 1? what effects do they have?

A

cocaine and tricyclic anti-depressants e.g. imipramine

cocaine can cause arrhythmias as increases cardiac function and raises blood pressure - more noradrenaline extracellularly and binding to effector.

43
Q

what are monoamine oxidase (MAO) and catechol o-methyltransferase (COMT)?

A

enzymes involved in metabolism of noradrenaline

44
Q

name 3 indirectly acting sympathomimetic amine drugs.

A

tyramine, ephedrine, amphetamine

45
Q

how do indirectly acting sympathomimetic amine drugs work?

A

cause reversal of noradrenaline transport through NAT so more release of noradrenaline into space

46
Q

MAOs have two main subtypes MAOa and MAOb. name a selective MAOb inhibitor.

A

selegine

47
Q

name 2 MAOIs (inhibitors).

A

phenelzine, iproniazid

48
Q

name a COMT inhibitor.

A

entacapone

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