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Semester 2 - Cardiovascular System > CVS S4 - The autonomic nervous system and the CVS > Flashcards

CVS S4 - The autonomic nervous system and the CVS Flashcards

1
Q

How is the resting membrane potential generated in cardiac cells?

A
  • At resting potential, K+ channels are open meaning the membrane is permeable to K+ ions
  • Movement of K+ ions out of the cell, down their concentration gradient established by the Na+-K+-ATPas and towards Ek creates a more negative voltage inside the cells
  • Resting potential = -90mV
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2
Q

Describe the phases of ventricular action potentials

A
  • Depolarisation occurs as Na+ channels open
  • Membrane potential increases to +20mV
  • Transient repolarisation occurs as voltage gated K+ channels open
  • Plateau phase as L-type Ca2+ channels open calcium influx equals potassium efflux
  • Repolarisation occurs as there is large K+ efflux and calcium channels become inactivated
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3
Q

Why does the cardiac muscle action potential peak at +20mV and not reach ENa?

A

Depolarisation stimulates the inactivation of voltage-gated sodium channels

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4
Q

What is the starting membrane potential in a pacemaker cell action potential?

A

-60mV

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5
Q

What are the ion channels responsible for the upstroke and downstroke of the pacemaker cells action potential?

A

Upstroke - Voltage gated calcium channels open

Downstroke - Voltage gated potassium channels open

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6
Q

What channel is responsible for the gradual depolarisation to threshold of the pacemaker potential and which ions flow through this channel?

A
  • HCN (hyperpolarisation- activated cyclic nucleotide gated channel)
  • Enables influx of sodium ions into the cell
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7
Q

Name the current created by the HCN channel and what does it do (depolarise?repolarise?etc)

A

If - Funny current

Gradual depolarisation of pacemaker cell to threshold -40mV

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8
Q

Outline the process of excitation-contraction coupling that occurs in the ventricular myocardium

A
  • Increase in intracellular calcium as depolarisation opens L-type calcium channels
  • This in turn stimulates calcium-induced-calcium-release (CICR)
  • Calcium bind to ryanodine receptors on the sarcoplasmic receptors releasing Ca2+ form SR stores
  • Calcium ions then bind to TnC (troponin) subunit on tropomyosin
  • Stimulates conformational change exposing myosin binding site on actin molecule
  • Sliding filament mechanism
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9
Q

Name an inhibitor of MLCK (smooth muscle excitation contraction coupling)

A

Protein kinase A (PKA)

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10
Q

Which enzyme opposes the action of MLCK? (smooth muscle excitation contraction coupling)

A

MLCP - Myosin light chain phosphorylase dephosphorylates the myosin head light chain

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11
Q

How are intracellular calcium levels returned to normal in cardiac myocytes?

A
  • Pumped back into the SR via SERCA

- Some exits the cell across the sarcolemma via PMCA or NCX

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12
Q

Where is the control centre for total peripheral resistance situated?

A

Vasomotor centres in the medulla oblongata in the brainstem

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13
Q

What two components make up control of total peripheral resistance?

A

Sympathetic nervous system and local metabolites

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14
Q

List some organs with high vasomotor tone

A

Skin, skeletal muscle, gut

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15
Q

What causes a decrease in vasomotor tone in skeletal muscle during exercise?

A
  • Mainly due to local release of vasodilator metabolites
  • Partly due to specialised vasodilator response to circulating levels of adrenaline mediated through beta-2-adrenoceptors
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16
Q

Outline concentration coupling in vascular smooth muscle

A
  • Initiated by depolarisation (opening voltage gated calcium channels) or activation by alpha 1 adrenoceptors (G alpha q subunit)
  • G alpha q activated phospholipase C
  • Cleaves PIP2 to forms IP3 and DAG
  • IP3 bind to receptors on sarcoplasmic receptors releasing calcium
  • Calcium binds with calmodulin which together as a complex activates myosin light chain kinase (MLCK)
  • MLCK phosphorylated the myosin light chain allowing myosin cross bridge to bind actin filament and allow contraction to occur
  • DAG activate protein kinase C which inhibits the effects of myosin light chain phosphatase (MLCP) which normally breaks the myosin cross bridge
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17
Q

Describe the differences between where neurones of the parasympathetic and sympathetic divisions synapse

A

Sympathetic- with post-ganglionic neurones in the paravertebral chain

Parasympathetic- with neurone in ganglia close to the target tissue

18
Q

How do nicotinic receptors on post-ganglionic neurones differ from muscarinic and adrenoreceptors

A

Nicotinic receptors have an integral ion channel

Adrenoreceptors and muscarinic receptors are G-protein coupled so have no integral ion channel

19
Q

What neurotransmitter molecule binds to muscarinic receptors?

A

Acetylcholine

20
Q

What is the parasympathetic input to the heart?

A

Pre-ganglionic fibres- 10th Cranial nerve (Vagus nerve)

21
Q

What receptors does the parasympathetic input act on and what are its general effects?

A
  • M2
  • Decreases heart rate (negative chronotrophic effect)
  • Decreases AV node conduction velocity
22
Q

What is the sympathetic input to the heart?

A

Post-ganglionic fibres from the sympathetic trunk

23
Q

What receptors do sympathetic input in the heart act on and what are its general effects?

A
  • Acts on beta-1-adrenoreceptors
  • Increases heart rate (positive chronotrophic effect)
  • Increases force of contraction (positive inotrophic effect)
24
Q

How does the sympathetic nervous system increase the speed of pacemaker potentials?

A
  • Mediated by beta-1-adrenoreceptors
  • Increases levels of cAMP
  • Causes more HCN channels to open
  • Increases the speed of depolarization
25
Q

How does the parasympathetic nervous system decrease the speed of pacemaker potentials?

A
  • Mediated by M2 receptors

- Increases K+ conductance and decreases cAMP

26
Q

How does the sympathetic nervous system increase the force of contraction in heart muscle?

A
  • Noradrenaline acts on beta-1-adrenoreceptors in myocardium (G alpha s)
  • Increases cAMP
  • In turn activates PKA
  • Causes phosphorylation of Ca2+ channels meaning they remain open for longer and so more calcium ions enter the cell during the action potential
  • Increases the force of contraction
27
Q

Which type of adrenoreceptor would be found in the majority of arteries and veins?

A

Alpha-1

28
Q

What effects does alpha-1 receptors in the vasculature mediate?

A
  • At pharmacological levels of adrenaline IP3 production is stimulated which increases calcium release from stores and causes increase efflux into the cell
  • Stimulates vasoconstriction
29
Q

What type of adrenoreceptor would be found in coronary and skeletal muscle blood vessels?

A

Beta-2-adrenoreceptors

30
Q

What effect do beta-2 adrenergic receptors found in skeletal and coronary blood vessels mediate?

A
  • Respond to circulating levels of adrenaline
  • Increases cAMP
  • Activates PKA
  • Opens K+ channels and inhibits MLCK
  • Causing vasodilation
31
Q

Describe the location and function of baroreceptors

A
  • High pressure side of system in carotid and aortic sinus
  • Excitation occurs by stretching under high pressure which is transmitted to the medulla oblongata via afferent nerve fibres
32
Q

Describe the function of the atrial volume receptors

A
  • Low pressure baroreceptors
  • Increase in volume is transmitted to the hypothalamus
  • Decreases production of ADH (vasopressin)
  • Leads to loss of water via urine, decreasing circulatory volume
33
Q

List three classes of drugs with important functions in the CVS

A
  • Sympathiomimetics
  • Adrenoreceptor antagonist
  • Cholinergics
34
Q

What is the function of dobutamine and what receptors would the drug act on?

A

Beta-1 agonist

Given in cardiogenic shock

35
Q

Give an example of a sympathiomimetic drug used outside the CVS and outline its function

A

Salbutamol

Acts on beta-2-adrenoreceptors in treatment of asthma

36
Q

Which drug would be given in the treatment of glaucoma and which class does this belong to?

A

Pilocarpine

Muscarinic agonist

37
Q

What is the function of prazosin?

A

Inhibits noradrenaline action on alpha-1 adrenoceptors causing vasodilation

38
Q

What are the functions of muscarinic antagonists?

A

Increase heart rate, bronchial dilation and dilate pupils for examination

39
Q

List two beta-adrenoreceptor antagonists and explain how they differ

A

Propanolol- non-sensitive so acts on both beta 1 and 2 receptors

Atenolol- specific to beta 1 receptors, reduces risk of bronchioconstriction

40
Q

How does the parasympathetic nervous system cause constriction of airways of the lung and what counteracts this effect?

A
  • Acetylcholine binds to M3 receptors causing constriction

- Circulating adrenaline causes dilation by binding to beta-2 adrenoreceptors

41
Q

List the effects of the sympathetic nervous system on the liver and how these effects are mediated

A

Noradrenaline stimulates glycogenolysis and gluconeogenesis by binding to alpha and beta-2 adrenoreceptors

42
Q

How does the action of the sympathetic nervous system differ between sweat glands on the palms of the hands from the rest of the body?

A
  • Sweat glands in the hand are stimulated by circulating adrenaline binding to alpha adrenoreceptors
  • Sweat glands located around the rest of the body are stimulated by acetylcholine binding to cholinergic muscarinic receptors

Semester 2 - Cardiovascular System (13 decks)

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