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PHSL 232 > L6 > Flashcards

L6 Flashcards

1
Q

what does intrinsic control effect

A

HR and SV

this is preload, afterload, and contractility

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2
Q

what is extrinsic control

A

hormonal and nervous controls

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3
Q

why do we need to be able to regulates our hearts excitability

A

because of the 4 F’s

fight, flight, feeding and fucking

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4
Q

where do the autonomic nerves come from

A

the brain stem

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5
Q

what is the parasympathetic nerve that innovates the heart called

A

the vagus nerve

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6
Q

where do the parasympathetic nerve fibers go to in the heart

A

the SA and AV node

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7
Q

what effect do parasympathetic fibers have on the heart

A

they only extend to the nodes and not the mussel itself therefore it only has an effect on the rate that the heart beats

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8
Q

what is the sympathetic nerve called that innovates the heart

A

the cardiac nerve

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9
Q

where do the sympathetic nerve fibers extend to

therefore leading to what effect

A

the nodes and the mussel therefore it has an effect on the HR and the contractility

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10
Q

what is contractility

A

changing the function of the heart without changing the EDV

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11
Q

what phases of excitation does autonomic nerve innovation effect

A

phase 4 and 3

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12
Q

explain the effect of sympathetic stimulation on pacemaker cells

A

noradrenaline is released onto the pacemaker cells, this binds to the b-adrenoceptors which through intracellular signaling causes more +ive charge to come into the cell

more +ive charge is coming into the cell making the slope of phase 4 steeper (reaching threshold of LTCC (-50, -40mV) faster

therefore the spontaneous rate of the SA node depolerisation is increased

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13
Q

what is it called when you increase the heart rate

A

tachycardia

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14
Q

describe the intracellular signalling pathway for sympathetic stimulation in pacemaker cells

A

noradrenaline binds to the b1-adrenoceptor which is coupled to adenylyl cyclase. when NA binds it activates adenylyl cyclase which then generates cAMP

cAMP directly regulates the funny Na+ channels therefore an increase in cAMP increases funny Na+ current

cAMP also activates protein kinase A which phosphorylate TTCC. this causes them to become more active meaning more Ca2+ comes into the cell

PKA also increases activity of K+ channels meaning that K+ is better able to leave the cell meaning that the cell is able to repolarise faster

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15
Q

what is the overall effect of parasympathetic stimulation of the heart

A

the spontaneous rate of the SA node depolerisation decreases

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16
Q

what is bradycardia

A

when the HR decreases

17
Q

describe the intracellular signalling pathway for parasympathetic stimulation

A

ACh binds to muscarinic receptors (M2), this inhibits adenylyl cyclase causing a fall in intracellular cAMP

this decreases the flow of Na through the funny Na channels and reduced PKA activity

less PKA = less Ca2+ through TTCC and reduced K+ current

HOWEVER the M2 receptor is coupled to a ACH sensitive K+ channel, therefore when ACH binds this channel opens causing hyperpolarisation

18
Q

the overall effects of para and sympathetic stimulation are…..

A

sympathetic = stronger and faster

parasympathetic = slower and weaker

19
Q

how come the SA node is known as the pacemaker of the heart when all of the cells are callable of generating action potentials

A

this is because the SA spontainiously fires at the highest rate

this means that although the other cardiac cells spontaneously fire, they never get the chance for those AP’s to be fired because they are always conducting the APs from the SA node

20
Q

what what rate does the AV node spontaneously fire

A

40-50BPM

21
Q

what what rate do the purkinje fibers spontaneously fire

A

20-30BPM

22
Q

what are chronotropic factors

A

factors that affect heart rate (things that cause tachycardia and bradycardia)

23
Q

what is proof that the sympathetic and parasympathetic systems are always tonically active in the heart

A

because the SA node fires at 110 BPM therefore if these weren’t tonically active resting heart rate would be 110BPM

24
Q

factors that affect contractility are called…..

A

inotropic factors

25
Q

how does sympathetic stimulation increase the strength of contraction

A

when noradrenaline binds to beta 1 receptor it activates PKA which phosphorylates LTCC and RyR (ca release from SR) therefore there is a large increase in intracellular Ca2+

it also phosphorylates Phospholamban (PLB). the phosphorylation releases the inhibition of SERCA mentioning that there is an increase in Ca uptake

it also phosphorylates troponin I (for inhibit) which limits the interaction of Ca with TnC which DECREASES TnC’s sensitivity to Ca

this is what allows for sympathetic to have a stronger and faster contraction

26
Q

Noradrenaline:

A. increases the Ca2+ sensitivity of the myofilaments

B. decreases the Ca2+ sensitivity of the myofilaments

C. causes dephosphorylation of PLB

D. causes dephosphorylation of RyR

A

B

27
Q

why would you want to decrease Ca sensitivity in myofilaments when you are trying to increase speed and strength of contraction

A

because it will dissociate quicker so the heart can relax faster. Because there is so much ca in the cell the weak binding doesn’t matter

Therefore it increases the speed of contraction and really increases the speed of relaxation

28
Q

what happens when the heart contracts in terms of the coronary vessels

A

when the heart contracts the heart squishes right down. this means that the coronary vessels get squishes so that no blood can get through then during systole

this is another reason why the heart needs to relax quickly during high HR because if the heart doesn’t spend sufficient time in diastole the cardiac cells wont get the appropriate coronary perfusion and the heart will die

29
Q

what is dromotropic

A

conduction speed

Increase conduction velocity so that we can get better synchronisation

30
Q

what is the difference between noradrenaline and adrenalin’s effect in the heart

A

noradrenaline is the neurotransmitter from the sympathetic nerve

adrenaline is the effect that a hormone has on the heart

however they causes the same things to happen intracellularly

neurotransmitter (nerve) vs hormone

31
Q

what are some hormones that have short term effects on the heart

A

catecholamines such as adrenaline, noradrenaline and dopamine.

glycosides such as digoxins/digitalis

32
Q

what is the effect of catecholamines and glycosides on the intracellular signaling pathways

A

catecholamines = the same as sympathetic pathway

glycosides inhibit Na/K ATPase

therefore they both change Ca signalling

33
Q

what are some long term inotropic regulators

A

angiotensin 2 (AT1 in heart)

endothelin (ET1 in the heart)

thyroid hormone (T3)

34
Q

describe the intracellular signalling pathway for glycosides

A

these inhibit Na/K ATPase meaning that na will build up in the cell

this then effects the Na/Ca exchanger as ca will not be able to be pumped out of the cell if it is not using the energy of Na coming down its conc gradient

this will initially increase the contractility of the heart

however when na gets really high it will reverse the exchanger to bring Ca into the cell so Na can leave

when this happens the heart will never be able to relax and you will die lol 🤣

35
Q

what would reverse the effects of glycosides

A

NCX

36
Q

Adrenaline decreases the Ca2+ sensitivity of the myofilaments

BECAUSE

adrenaline leads to phosphorylation of RyR

A.Both statements are true and causally related

B.Both statements are true but not causally related

C.First statement is true and second is false

D.Second statement is true and first is false

E.Both statements are false

A

B

37
Q

what are some negative inotropic factors

A

ACh

Ca channel blockers

beta blockers (b-adrenoceptor blockers)

38
Q

why would you want to decrease the contractility of the heart (inotropic factors)

A

you do this because it is about energy expenditure of the heart

when you are in heart failure the heart is very inerfishent therefore it uses a lot of ATP

therefore you give inotropic factors to put less stress on the heart by reducing ATP at the cost of causing the heart to beat less strongly

39
Q

describe the intracellular signaling pathways for beta blockers

A

they block the b-adrenoceptor therefore reducing cAMP levels –> reducing PAK activity ect

the lack of phosphorylation of TnI means that tropomyosin C is more sensitive to Ca which reduces the need for ATP meaning that there is less stress on the heart

PHSL 232 (30 decks)

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