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I've got hypertension > Lecture 6 > Flashcards

Lecture 6 Flashcards

1
Q

How can we control the heart extrinsically?

A

Via hormonal and nervous control

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2
Q

What four things to we need autonomic control of the heart for?

A
  • fight
  • flight
  • feeding
  • sexy times
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3
Q

The heart is controlled both _____________ and _____________

A

sympathetically

parasympathetically

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4
Q

What is the name of the nerve that innervates the heart sympathetically?

A

sympathetic cardiac nerve

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5
Q

What is the name of the nerve that innervates the heart parasympathetically?

A

the vagus nerve

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6
Q

The vagus nerve releases what to innervate the heart parasympathetically?

A

ACh

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7
Q

The sympathetic cardiac nerve releases what to innervate the heart sympatheically?

A

NE

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8
Q

What is the function of altering the heart autonomically?

A

to alter the function without changing the end diastolic volume

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9
Q

What does the vagus nerve innervate to control the heart parasympathetically?
What does this allow it to control?

A

the SA node and the AV node

this is to control the heart rate (not the cardiac muscle cells themselves)

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10
Q

What does the sympathetic cardiac nerve innervate to control the heart sympathetically?

A

the SA node, the AV node and the muscle fibres to control both heart rate and contractility

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11
Q

Why can the events stack?

A

Because increasing the preload increases the end-diastolic volume and increasing the contractility increases the end systolic volume

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12
Q

What is the spontaneous rate of action potentials in an atrial cell?

A

110bpm

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13
Q

What is the resting heart rate?

A

60-70bpm

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14
Q

Why is it that the spontaneous rate of action potentials in an atrial cell is 110bpm but the resting heart rate is 60-70bpm?

There must be ________ of the ___________ cells to slow their rate from _________ to _________ because there is constant release of ________ or ___________ into the ____________ node

A

There must be control of the pacemaker cells to slow their rate from 110bpm to 60bpm because there is constant release of NE or ACh into the SA node

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15
Q

What are sympathetic fibres also known as?

A

cardiac nerves

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16
Q

What are parasympathetic fibres also known as?

A

the vagus nerve

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17
Q

If you can change the _______ of phases 4 and 3 in the action potential for a ventricular cell, you are going to be able to make the what go up or down?

A

slope

the heart rate

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18
Q

What happens during phase 4 of the action potential of a pacemaker cell?

A

The resting membrane potential is -60mv/-70mV and it is unstable due to the funny Na+ channels. There is a slow influx of Na+ and then the opening of T-type Ca2+ channels. The threshold is reached at -50mV/-40mV. An action potential is generated and then there is repolarisation of the cell through K+ channels

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19
Q

How can neuronal control affect the action potential of a pacemaker cell? (sympathetic stimulation)

A

Sympathetic cardiac nerve releases NE onto the pacemaker cells which bind to β-adrenoreceptors which will open Ca2+ and Na+ channels. This lets more + charge into the cell so the resting membrane potential becomes more +
Also, the phase 4 line is going to be steeper. We are therefore starting from a less negative potential and we are depolarising more quickly

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20
Q

If we increase the spontaneous rate of SA node depolarisation, the heart rate is going to what?

A

increase

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21
Q

What is an increase in the heart rate called?

A

Tachycardia

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22
Q

What is the cellular effect of NE binding the β1-adrenoreceptors on the pacemaker cells?

A

The β-adrenoreceptors is coupled to adenyl-cyclase which generate cAMP. This is secondary signalling molecule and it directly activated the funny Na+ channels and the more Na+ they let into the cell.
cAMP also activates PKA which activates T-type Ca2+ channels which makes them more active so more Ca2+ gets into the cell. It also phosphorylates K+ channels

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23
Q

Why is it important that NE binding to the β-adrenoreceptors phosphorylates K+ channels which opens them?

A

Because if more + charge can now leave the cell, the slope of the 3rd phase is steeper so the cell is repolarising more quickly, ready for the next beat
this will also increase the heart rate

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24
Q

How can neuronal control affect the action potential of a pacemaker= cell? (parasympathetic stimulation)

A

The vagus nerve releases ACh onto the pacemaker cells which bind to muscarinic which will open K+ channels and inhibit Na+ and Ca2+ channels. This lets less + charge into the cell so the resting membrane potential becomes more -
Also, the phase 4 line is going to be flatter. We are therefore starting from a more negative potential and we are depolarising less quickly
There is an increased gap between successive action potentials and so the heart rate is decreased

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25
Q

If we decrease the spontaneous rate of SA node depolarisation, the heart rate is going to what?

A

decrease

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26
Q

What is a decrease in heart rate called?

A

Bradycardia

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27
Q

What is the cellular effect of ACh binding the muscarinic on the pacemaker cells?

A

When ACh binds to the muscarinic receptor, it too is associated with adenyl-cyclase but the binding inhibits the action of adenyl-cyclase. This means that there is a decrease in cAMP. This means there will be less direct stimulation of the funny Na+ channels so the current through them goes down. There is also going to be less phosphorylation of PKA so there is less phosphorylation of T-type Ca2+ channels so phase 4 sloe is going to be less steep. There is also less activation of the K+ channels

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28
Q

Why is it important that ACh binding to the muscarinic receptors phosphorylates K+ channels which inhibits them?

A

The K+ channels responsible for the repolarisation phase are going to be less active.
BUT this is countered by the fact that we get activation of another set of K+ channels. These are directly coupled to the muscarinic receptors and these become more active. This allows K+ to come out of the cell more quickly, making the cell more - charged so the heart rate decreases

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29
Q

If every cell can conduct action potentials, why is it that the SA node cells that set the heart rate?

A

because these cells go faster than all other cell types and it suppresses the others

30
Q

Why can the AV node not set the heart rate?

A

because they only conduct action potentials to create a heart rate of 40-50bpm and so the SA node conducts an action potential before they spontaneously depolarise but if the SA node stopped working, the SA node and purkinje fibres could take over

31
Q

What are the sympathetic and parasympathetic controls of the heart rate collectively known as what?

A

chronotropic factors

32
Q

Without parasympathetic innervation of the heart, what would the heart rate be?

A

110bpm

33
Q

How does the sympathetic innervation affect the contraction?

A

Sympathetic activation means to more and faster Ca2+ release, faster cross-bridge cycling, more and faster Ca2+ uptake. This means that there is stronger ad faster contraction and faster relaxation

34
Q

All the things that are changing that are affecting contractility are referred to as what?

A

inotropic factors

35
Q

All the things that are changing that are affect duration of contraction and relaxation are referred to as what?

A

lusitropic factors

36
Q

How does the sympathetic activation affect the contraction from a cellular level?

A

The sympathetic cardiac nerve releases NE which increases cAMP to activate PKA. PKA phosphorylates

  • L-type Ca2+ channels which increase [Ca2+]
  • RyR which increases SR Ca2+ release
  • TnI which limits the interaction of Ca2+ with TnC which DECREASES Ca2+ sensitivity
  • PLB which stops SERCA inhibition which increases SR Ca2+ uptake
37
Q

Increased contractility means higher SV for the same ______ which means we shift to a _______ Starling curve

A

end-diastolic volume

higher

38
Q

What is the effect of NE?

a. increases the Ca2+ sensitivity of the myofilaments
b. it decreases the Ca2+ sensitivity of the myofilaments
c. it causes dephosphorylation of PLB
d. it causes dephosphorylation of RyR

A

It decreases the Ca2+ sensitivity of the myofilaments

39
Q

Why is it important that NE decreases the Ca2+ sensitivity of the myofilaments?

A

this means the contraction is weaker (bad) but it does mean that the Ca2+ dissociates from the troponin faster which relaxes the heart faster

40
Q

At rest, what percentage of the time does the heart spend in diastole and what percentage is spent in systole?

A

66% in diastole

33% in systole

41
Q

At a high heart rate, what percentage of time does the heart spend in diastole and what percentage is spent in systole?

A

33% in diastole
66% in systole

(remember less time is spent in both because the cycle only lasts 0.33s)

42
Q

If we allow diastole to occur really quickly at high heart rates, we need to allow ______ to occur really quickly. What does this mean for the Ca2+ sensitivity of the myofilamtnets?

A

relaxation

this is why you need to decrease the Ca2+ sensitivity of the myofilaments allowing the heart to contract more quickly and relax more quickly

43
Q

The quick relaxation of the heart maintains what?

A

appropriate ventricular filling during diastole

44
Q

When does the coronary circuit receive most of its flow?

Why is this?

A

during diastole

because when the heart is contracting, the coronary circulation will be squashed so blood flow through the coronary vessels stops during systole

45
Q

What is the issue with the coronary circuit receiving blood flow during diastole when the heart rate increases?

A

At a high heart rate, the length of systole decreases and so there is less time for the cardiac muscles to get the O2 and nutrients which will lead to coronary artery death

46
Q

Give an example of a positive chronotropic effect of sympathetic stimulation of the heart?

A

increase in heart rate

47
Q

Give an example of a positive inotropic effect of sympathetic stimulation of the heart?

A

elevated contractility

48
Q

Give an example of a lusitropic effect of sympathetic stimulation of the heart?

A

reduction in duration of diastole and systole

49
Q

Give an example of a dromotropic effect of sympathetic stimulation of the heart?

A

increase in conduction velocity

50
Q

Sympathetic stimulation of the heart leads to better synchronisation of what?

A

atrial and ventricular contractions

51
Q

Chronotropic effects refer to what?

A

rhythmic excitation and heart rate

52
Q

Inotropic effects refer to what?

A

strength of contractile force and blood pressure

53
Q

Dromotropic effect refer to what?

A

conduction speed

54
Q

As well as nervous control, the heart rate is controlled extrinsically by what?

A

hormones

55
Q

What are the two hormones that extrinsically control heart rate and what do these each do?

A
  • adrenaline which increases HR
  • ACh which decreases HR

these change the membrane potential and the rate of depolarisation, just like the nervous control

56
Q

As well as changing heart rate, hormones can also change what?

A

contractility

57
Q

Which hormone is responsible for increasing contractility (positive inotropic effect)?

A

adrenaline

58
Q

In the short term, what is the effect of the release of catecholamines such as adrenaline or dopamine on contractility?
What is the mechanism?

A

they will increase it by the same mechanism as noradrenaline at the nerve terminals

59
Q

As well as due to catecholamines, we can also get increase in contractility due to drugs such as what? What do these do?

A

glycosides
(digoxins/digitalis)

these change Ca2+ signalling

60
Q

What are three long term changers of contractility?

A

Angiotensin ||
Endothelin
Thyroid hormone

61
Q

How does adrenaline (hormone) stimulate contraction at the cellular level?

A

Adrenaline binds to the β-adrenoreceptor which causes a rise in cAMP. This activates PKA and PKA phosphorylates

  • L-type Ca2+ channel which increases [Ca2+]
  • RyR which increases SR Ca2+ release
  • TnI which limits the interaction of Ca2+ with TnC which DECREASES Ca2+ sensitivity
  • PLB which releases SERCA inhibition which increases the SR Ca2+ uptake
62
Q

How do drugs (glycosides) lead to a short term increase in heart rate?

A

These inhibit the Na+/K+ ATPase. It is this pump that is keeping the Na+/Ca2+ exchanger working (this pump uses the Na+ gradient created from the Na+/K+ ATPase to get Ca2+ out of the cell).
If Na+/K+ ATPase is inhibited, Na+ is not being pushed out which means that it is harder for Na+ to enter and therefore it is harder for Ca2+ to leave. Ca2+ accumulates in the cell which initially increases the function of the heart

63
Q

What is the purpose of the Na+/Ca2+ exchanger?

A

this is a way to get Ca2+ out of the cell by using the driving force bringing Na+ into the cell
this Na+ gradient is formed from the Na+/K+ ATPase

64
Q

What is the purpose of Na+/K+ ATPase?

A

It pushes Na+ out of the cell and K+ into the cell and this creates a Na+ gradient which is used to push Ca2+ out of the cell

65
Q

Why are glycoside drugs bad in the long term?

A

Because they lead to a build up of Na+ in the cell which means that eventually the gradient for Na+ switches so instead of Na+ coming into the cell, it leaves via Na+/K+ exchanger. If Na+ is leaving the cell, Ca2+ comes in via the Na+/Ca2+ exchanger and we have lost the ability to get Ca2+ out of the cell. This means it will never dissociate from TnC and the heart won’t stop contracting (bad)

66
Q

Adrenaline decreases the Ca2+ sensitivity of the myofilaments BECAUSE adrenaline leads to phosphorylation of RyR

A

Both statements are true but not causally related

67
Q

Which hormone (and other things) is responsible for decreasing contractility (negative inotropic effect)?

A

acetylcholine

Ca2+ channel blockers
β - Blockers

68
Q

How do Ca2+ channel blockers decrease contractility?

A

They block the Ca2+ from entering the cell so there is less Ca2+ to drive contraction. There is also less Ca2+ coming in to activate the RyR so there is less Ca2+ coming out of the SR. The amount of Ca2+ in the cell goes down so there is lower levels of contraction

69
Q

How does ACh (hormone) reduce contraction at the cellular level?

A

This binds to the muscarinic receptors which decreases the cAMP which means there is less PKA activity. This means there is less activation of

  • L-type Ca2+ channels so there is a decrease in Ca2+
  • RyR which means there. is a decrease in SR Ca2+ activity
  • TnC which means there is an INCREASE in Ca2+ sensitivity
  • PLB which increases SERCA inhibition so there is a decrease in SR Ca2+ uptake
70
Q

How do β - Blockers lead to a decrease in contractility?

A

They block the β-adrenoceptor which reduces cAMP so there is less PKA activity and hence reduced activity of LTCC, RyR and SERCA
It also increases the Ca2+ sensitivity of TnC. It reduces the need for ATP because there is less Ca2+ in the cell and therefore there is less stress on the heart

71
Q

What is the effect of digitalis, a glycoside, on Ca2+ sensitivity of the myofilments?

A

it remains unchanged

I've got hypertension (47 decks)

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