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Semester 2 > CVS Session 4 > Flashcards

CVS Session 4 Flashcards

0
Q

Which channels in the CSM are open at rest?

A

Inward rectifier potassium channels

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1
Q

What is the main factor causing establishment of the resting membrane potential?

A

Potassium permeability of the CSM at rest

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2
Q

Why is the resting membrane potential of a cardiac myocyte -90 mV and not Ek (-95 mV)?

A

Small permeability of CSM to other ions

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3
Q

Between which two equilibrium potentials does the membrane potential of a ventricular myocyte stay within throughout an action potential?

A

Sodium (+30 mV)

Potassium (-90 mV)

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4
Q

How long does a ventricular action potential last?

A

~280 ms

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5
Q

What determines the point of plateau in a ventricular action potential?

A

Myocyte type

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6
Q

What causes the upstroke of a ventricular action potential?

A

Opening of V-G sodium channels –> sodium influx

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7
Q

What two events cause the initial repolarisation of the ventricular action potential?

A

Transient V-G outward potassium channels –> potassium efflux
Reversal of NCX caused by depolarisation –> small -ve current

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8
Q

What causes the plateau of action potential in a ventricular cardiac myocyte?

A

Opening of V-G L-type calcium channels –> calcium influx balanced w/ potassium efflux

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9
Q

What causes repolarisation of the ventricular action potential?

A

V-G potassium channels –> potassium efflux

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10
Q

How do V-G potassium channels vary?

A

Depend on myocyte present - different types behave differently contributing differently to electrical properties of the myocyte

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11
Q

How is the membrane potential of SAN cells described?

A

Unstable

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12
Q

What is the pacemaker potential?

A

Slow depolarisation to threshold

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13
Q

What initiates Ip?

A

Membrane potential more -ve than -50 mV activating hyperpolarisation-activated cyclic-nucleotide (HCN) gated channels

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14
Q

What do HCN channels do?

A

Allow sodium influx at SAN myocyte membrane potential

Also potassium influx at other potentials

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15
Q

How can the activation of the pacemaker potential be increased?

A

A more -ve membrane potential

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16
Q

After threshold has been reached, what causes the upstroke of the SAN action potential?

A

Opening of V-G calcium channels –> calcium influx

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17
Q

What causes the downstroke of the SAN action potential?

A

Opening of V-G potassium channels –> potassium efflux

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18
Q

Why do pacemaker cells not require innervation?

A

They do not sit at rest so have natural automaticity

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19
Q

Why is the SAN the ‘master pacemaker’?

A

It is fastest to depolarise so sets rhythm of contraction

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20
Q

What will take over the pacemaker function of the SAN if it is compromised?

A

AVN

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21
Q

How are the action potential graphs of the SAN and AVN related?

A

Similar shape but AVN is over a longer period of time

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22
Q

How are the action potential graphs of atrial muscle, Purkinje fibre and ventricular muscle cells related?

A

All similar shape w/ resting potential around -80 mV

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23
Q

What is the approximate resting membrane potential of the pacemaker cells?

A

-50 mV

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24
Q

What gives cardiac muscle cells mechanical strength?

A

Glycoprotein that spans membrane and crosses gap b/w cells - desmosome

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25
Q

What facilitates electrical coupling of cardiac cells?

A

Connexon subunits on both sides of membrane forming non-specific pore - gap junction

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26
Q

What is the function of intercalated disks?

A

To join cardiac muscle cells

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27
Q

Describe the nucleus in a cardiac muscle cell.

A

Single

Central

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28
Q

What releases 25% of the calcium needed for the sliding filament model in cardiac muscle cells?

A

Depolarisation opening L-type calcium channels in T-tubules

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29
Q

What causes calcium-induced calcium release?

A

Localised increase in calcium concentration opens CICR channels in sarcoplasmic reticulum

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30
Q

Why is there a close link b/w L-type calcium channels and CICR channels in cardiac muscle cells?

A

Cardiac tissue needs actual calcium influx for contraction

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31
Q

What function does calcium perform during contraction of the cardiac muscle cell?

A

Binds to TnC –> conformational tropomyosin change –> reveals myosin binding site on actin

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32
Q

What function does calcium have during diastole?

A

Increased calcium concentration stimulates SERCA –> calcium moves into SR –> sarcolemmal calcium ATPase and sodium/calcium exchanger pump calcium out of the cell through the CSM

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33
Q

How is the tone of BV controlled?

A

Smooth muscle cells in tunica media of arteries, arterioles and veins

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34
Q

How do the actin filaments in myocytes of BV compare to those in other cells?

A

Longer so can shorten cell more

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35
Q

How are actin filaments in BV myocytes anchored within the cell?

A

Dense bodies

Bonds

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36
Q

What can cause excitation-contraction coupling of BV myocytes?

A

Depolarisation

Activation of GPCRs

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37
Q

How does depolarisation cause excitation-contraction coupling?

A

Allows entry of calcium through calcium channels

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38
Q

What class of GPCRs are activated in excitation-contraction coupling?

A

Alpha-adrenoreceptors

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39
Q

Give a brief overview of the activation of GPCRs causing excitation-contraction coupling.

A

IP3 acts as calcium channel –> SR releases calcium –> calcium binds to calmodulin instead of TnC –> MLCK activated which phosphorylates regulatory light chain on myosin head –> actin-myosin interaction

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40
Q

What affect does decreasing calcium levels have on myosin light chain phosphatase?

A

Causes it to dephosphorylate the myosin light chain –> no interaction –> relaxation

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41
Q

What is PKA?

A

Protein Kinase A - phosphorylates MLCK therefore inhibiting contraction as it prevents it phosphorylating the light chain on myosin head

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42
Q

What is PKA regulated by?

A

cAMP

43
Q

Why does the contraction of a BV myocyte last longer than in other myocytes?

A

Attachment formed during contraction can become locked

44
Q

What does the ANS exert control over?

A

Vascular and visceral smooth muscle
Exocrine secretion
Rate and force of contraction of the heart

45
Q

What are enteric neurones usually controlled by?

A

Sympathetic and parasympathetic nerve fibres

46
Q

Where do parasympathetic neurones synapse?

A

In ganglia close to target tissue

47
Q

How do the lengths of the pre- and post-ganglionic nerve fibres compare?

A

Long pre-

Short post-

48
Q

Which neurotransmitter and relative receptor do parasympathetic post-ganglionic neurones usually use

A

ACh

Muscarinic

49
Q

What is the exception to the usual rule of sympathetic post-ganglionic neurones being noradrenergic?

A

Sweat glands using ACh and muscarinic receptors

50
Q

Where do sympathetic neurones synapse?

A

Mostly in paravertebral chain but can travel up or down chain before synapsing

51
Q

How do preganglionic neurones of both sympathetic and parasympathetic divisions transmit action potentials?

A

Release ACh –> binds to nicotinic receptors on post-ganglionic cell –> opens ion channel –> influx of sodium –> depolarisation –> AP down neurone

52
Q

How are chromaffin cells like specialised post-ganglionic symoathetic neurones?

A

ACh from the preganglionic neurone acts directly on the cell to release adrenaline directly into the bloodstream

53
Q

What do NA and adrenaline act on?

A

GPCRs with no integral ion channel - adrenoreceptors

54
Q

What allows for diversity and selectivity of drug action at adrenoreceptors?

A

Different tissues have different subtypes

55
Q

How do parasympathetic postganglionic neurones transmit action potentials?

A

Release ACh –> binds to muscarinic receptors on effector cells (GPCRs)

56
Q

What two methods of action can be used to treat asthma?

A

Stimulate beta-2

Inhibit M3

57
Q

What are the sympathetic and parasympathetic effects on the pupil of the eye and their relevant receptors?

A

S - dilation (contract radial muscle); alpha-1

P - contraction (contracts sphincter muscle; M3

58
Q

What are the sympathetic and parasympathetic effects on the airways of the lungs and their relevant receptors?

A

S - relax; beta-2

P - contract; M3

59
Q

What are the sympathetic and parasympathetic effects on the heart and their relevant receptors?

A

S - increase rate and force of contraction; beta-1

P - decrease rate; M2

60
Q

What are the sympathetic and parasympathetic effects on sweat glands and their relevant receptors?

A

S - localised secretion; alpha-1
S - generalised secretion; M3
P - no effect

61
Q

Why does increased sympathetic activity to the heart not have to increase activity elsewhere?

A

Drive to different tissues is independent and is only coordinated when needed, e.g. fight or flight

62
Q

Does the ANS initiate electrical activity in the heart?

A

Nope

63
Q

Which preganglionic fibres transmit the parasympathetic input to the heart?

A

X cranial nerve - vagus nerve

64
Q

Where does the vagus nerve synapse?

A

W/postganglionic cells on epicardial surface

W/in walls of heart at SAN and AVN

65
Q

Why does parasympathetic input to the heart not really affect force of contraction?

A

Doesn’t synapse much w/postganglionic cells in ventricles

66
Q

What affect does the binding of ACh released from postganglionic cells to M2 receptors have in parasympathetic innervation of the heart?

A

-ve chronotropic effect

Decreased AVN conduction velocity

67
Q

How does the sympathetic division innervate the heart?

A

Long postganglionic fibres from the sympathetic trunk innervate the SAN, AVN and myocardium –> release NA

68
Q

What does binding of NA to beta-1 adrenoreceptors cause in the sympathetic input to the heart?

A

+ve chronotropic effect

+ve inotropic effect

69
Q

What must be altered to alter pacemaker cell contraction rate?

A

Slow depolarising pacemaker potential

70
Q

What assists the HCN channels in the action of the funny current?

A

T-type sodium channels

71
Q

How does the sympathetic branch of the ANS act on pacemaker potentials?

A

Activates beta-1 receptors –> G-alpha-S activated –> stimulates adenylate cyclase –> increases cAMP –> speeds up pacemaker potential

72
Q

How does the parasympathetic branch of the ANS effect the pacemaker potential?

A

Activates M2 receptors –> G-alpha-1 activated –> inhibits adenylate cyclase –> decreases cAMP –> increases potassium conductance –> slows down pacemaker potential

73
Q

How does NA increase the force of contraction of the heart?

A

Beta-1 receptors activated –> increased cAMP –> PKA activated –> calcium channels activated so more calcium during action potential –> more SR calcium uptake so more CICR and increased sensitivity of contractile machinery to calcium

74
Q

What is the exception to the general rule that most BV receive sympathetic innervation?

A

Erectile tissue

75
Q

What class of receptors is present in most arteries and veins and is abundant in arterioles?

A

Alpha 1-adrenoreceptors

76
Q

What class of receptors are found in coronary and skeletal muscle vasculature as well as alpha 1-adrenoreceptors?

A

Beta 2-adrenoreceptors

77
Q

How does varying the sympathetic output to vasculature alter the vasomotor tone?

A 
Decrease = vasodilation
Normal = vasomotor tone
Increase = vasoconstriction
78
Q

What is needed in vasculature in order for there to be constriction?

A

Basal level of contraction

79
Q

What is the effect of NA and circulating adrenaline in BV w/alpha 1 and beta 2-adrenoreceptors?

A

NA - contraction

Adrenaline - vasodilatation

80
Q

How does adrenaline cause vasodilatation at physiological concentration?

A

Higher affinity for beta 2-adrenoreceptors –> increases cAMP –> activates PKA –> opens potassium channels and inhibits MLCK –> relaxation of smooth muscle

81
Q

How can adrenaline cause vasoconstriction at pharmacological concentrations?

A

Activates alpha 1-adrenoreceptors –> activates G-alpha-Q –> stimulates IP3 production –> increased calcium concentration from stores and influx –> smooth muscle contracts

82
Q

What has a stronger vasodilatation effect than activation of beta 2-adrenoreceptors?

A

Local metabolites

83
Q

Give some examples of local metabolites.

A

Adenosine
Potassium
Hydrogen ions
p(carbon dioxide)

84
Q

What is more important for ensuring adequate perfusion of skeletal and coronary muscle than activating beta 2-adrenoreceptors?

A

Local metabolites

85
Q

What communicates changes in the state of the CVS to the brain?

A

Afferent nerves

86
Q

What are baroreceptors?

A

Nerve endings in carotid sinus and aortic arch sensitive to stretch

87
Q

Which two types of receptors detect low pressure and high pressure system changes in BP and alter activity of efferent nerves as a result?

A

High pressure side - baroreceptors

Low pressure side - atrial receptors

88
Q

What is the baroreceptors reflex?

A

Increase mean arterial pressure detected by baroreceptors, communicated by afferent pathway to medulla –> coordinates efferent pathways in heart and vessels to cause bradycardia and vasodilatation

89
Q

Which nerves do afferent fibres travel up?

A

Vagus

Glossopharyngeal

90
Q

What three types of drugs are used which act on the ANS?

A

Sympathomimetics
Adrenoreceptor antagonists
Cholinergics

91
Q

What two types of molecule make up the sympathomimetic class of drugs?

A

Alpha-adrenoreceptor agonists

Beta-adrenoreceptor agonists

92
Q

What do sympathomimetics mimic?

A

Sympathetic nervous system

93
Q

Name three examples of sympathomimetics.

A

Adrenaline
Dobutamine
Salbutamol

94
Q

How is adrenaline used to treat cardiac arrest and anaphylactic shock?

A

Cardiac arrest - vasoconstriction to maintain BP

Anaphylactic shock - stimulates alpha 1 receptors to counteract widespread vasodilatation

95
Q

What method of action does Dobutamine follow?

A

Beta 1-agonist given in cardiogenic shock (pump failure)

96
Q

How does salbutamol work?

A

Beta 2- agonist specific to airway of lungs to cause dilation, doesn’t increase HR

97
Q

Name three examples of adrenoreceptor antagonists.

A

Prazonin
Propranolol
Atenolol

98
Q

How does prazonin work?

A

Alpha 1-antagonist –> inhibits NA action on vascular smooth muscle –> vasodilation –> antihypertensive

99
Q

How does propranolol work?

A

Non beta1/2 selective adrenoreceptor antagonist which acts at beta 1 to slow heart rate and force of contraction and at beta 2 to cause bronchoconstriction

100
Q

How does atenolol work?

A

Selective beta 1-antagonist given after MI to reduce cardiac workload with less risk of bronchoconstriction

101
Q

Give three examples of Cholinergics.

A

Pilocarpine
Atropine
Tropicamide

102
Q

How does pilocarpine work?

A

Muscarinic agonist which acts on constrictor pupillae muscle to treat glaucoma

103
Q

How do atropine and Tropicamide work?

A

Muscarinic antagonists which increase heart rate and bronchial dilation
Can be used to dilate pupils for eye examination

104
Q

How is the heart normally controlled?

A

Vagal control w/parasympathetic dominated control

105
Q

What happens if you pharmacologically block the autonomic control to the heart?

A

Rate increases towards intrinsic heart rate = 100 bpm

Semester 2 (45 decks)

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