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PHSL 232 > L4 > Flashcards

L4 Flashcards

1
Q

what is the contractile unit of a muscle cell

A

the sarcomere

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2
Q

do the peaks on the ECG happen before or after the contraction in the heart

A

before

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3
Q

what kind of event is an excitation contraction coupling

A

electro mechanical as electrical and mechanical activity overlap in time

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4
Q

what are the major components of excitation contraction coupling

A

Ca2+ entry

contraction (the contractile machinery)

getting the Ca out of the cells

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5
Q

what causes Ca entry

A

the cell membrane depolarises causing the membrane potential to rise

when this reaches the threshold for L type Ca channels they open and Ca enters the cell

the influx of Ca into the cell binds to the ryanodine receptor Ca2+ releasing channels (RYR2) which triggers the release of Ca form the SR

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6
Q

why do you get Ca2+ induced Ca2+ release

A

the density of RYR2 is very high near LTCC and the distance between them is very small (10 -20nm)

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7
Q

where does most of the Ca come from for the contraction

what channels does it come through

A

about 75% comes from the SR with only 25% coming from the extracellular environment through the LTCC

this difference is even larger agon in smaller mammals

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8
Q

in cardiac muscle, depolerisation causes….

A) direct opening of Ca2+ release channels (RYR2) on the SR

B) Ca induced Ca release

C) increased intracellular CA from 1 mM to 10 mM

D) opens funny Na channels

A

B

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9
Q

what is the extracellular concentration of Ca

A

2 mM

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10
Q

what is the intracellular concentration of Ca

A

0.001 mM

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11
Q

what is the concentration of Ca in the cytosol

A

0.1 - 1 uM

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12
Q

what causes contraction

A

Ca binds to troponin C

tropomyosin moves and acting and myosin interact

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13
Q

what are the 3 parts of the troponin complex

A

TnC = Ca binding domain

TnI = inhibitory domain

TnT = tropomyosin binding domain

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14
Q

what sequence causes the sarcomere to shorten

A

Actin binding sites are blocked until Ca2+ binds to TnC which causes the displacement of Troponin-Tropomysin

Interaction Actin-Myosin = cross-bridge

Myosin heads flips – ratchet action

Actin moves toward center
of sarcomere

Sarcomere shortens
Actin and Myosin don’t

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15
Q

describe the cross bridge cycle

A

ATP bound to Myosin split in ADP and Pi

Myosin has high actin affinity

Ca2+ increases, binds to
TnC, opens binding
place, Myosin moves to
Actin and binds

Energy released (ADP + Pi)
and Myosin head shifts from
90 to 45 degrees. this is the powerstroke

Ca2+ decreases, ATP binds,
Myosin has low actin affinity,
cross-bridge detaches

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16
Q

what is the sliding filament theory

A

Myosin is pulling actin towards center of the sarcomere.

Actin filaments slide along adjacent myosin filaments by cycling of cross-bridges with myosin

Z lines come closer together and cell shortens thus
producing force or tension

17
Q

how many myosin heads are there on a myofilament

A

600

18
Q

what increases the strength of contraction of the heart

what rest what % of cross bridges are formed

A

Contraction more forceful due to increase in the number of cross-bridges, and not due to more contracting cardiomyocytes

normally cross bridge cycling happens at about 20-40% meaning that it is possible to recruit more myofilament

19
Q

During contraction of the sarcomere:

A. Myosin is pulling actin towards the center of the sarcomere

B. Myosin shortens moving actin towards the center of the sarcomere

C. Actin shortens causing the z-lines to move towards the center of the sarcomere

D. Both actin and myosin shorten

A

A

20
Q

what is relaxation

A

it is the end of the contraction as Ca influx ceases

the SR is no longer stimulated to release Ca

and the cytosolic Ca must be rapidly reduced

21
Q

what are the 3 different mechanisms to reduce intracellular Ca

A

SERCA

Na/Ca exchanger

Ca ATPase

22
Q

describe how the SERCA pump decreases intracellular Ca levels

A

SERCA is ATP-dependent and pumps cytoplasmic Ca2+ back into SR (75% which is what the SR released to keep it balanced)

SERCA activity is regulated by Phospholamban (PLB),
PLB protein phosphorylation stimulates Ca2+ uptake as it removes the inhibition on the SERCA pump

23
Q

describe how the Na/Ca exchanger (NCX) pump decreases intracellular Ca levels

A

Na+ / Ca2+ exchange pump, driven by Na+ gradient (cotransport = secondary transporter)

this is responsible for getting rid of 24% of the intracellular Ca levels

24
Q

describe how the Ca ATPase pump decreases intracellular Ca levels

A

PMCA - plasma membrane Ca atpase

it is located in the membrane and uses ATP to pump Ca out of the cell

this is what gets the remaining 1% of Ca out of the cell

25
Q

what makes cardiomyocytes inexitable

2 reasons

A

“Stable” Ca2+ plateau makes cardiomyocytes inexcitable

they also have long absolute (250ms) and relative refractory periods (300ms) which prevents re-excitation during most of contraction period. it also prevents circuitous recycling of APs

26
Q

how long is the absolute refractory period in a cardiomyocyte

A

250ms

27
Q

how long is the relative refractory period in a cardiomyocyte

A

300ms

28
Q

why do cardiomyocytes need to have long periods of time where that are inexcitable

A

It has a long refectory phase because it needs to be relaxed so that the heart can be filled with blood again then it wouldn’t function (it would be in tetanus and you would die)

Therefore in the heart summation is not possible because the heart has to completely relax

29
Q

how much ATP does the heart make in a day

A

3.5 - 5 kg per day

30
Q

what kind of metabolism does the heart use

A

aerobic metabolism (oxidation)

31
Q

what % of the hearts energy comes from oxidising fatty acids

A

60 - 75%

32
Q

what % of the hearts energy comes from oxidising glucose

A

25 - 40%

33
Q

what suplys O2 to the heart

A

coronary circulation

34
Q

at the heart O2 extraction from the blood is very high. what % of O2 is extracted

A

75%

35
Q

the heart is very vulnerable to coronary ear disease/ischemia, why is this

A

When you look at these vessels they have a feather like appearance over the heart as there is a capillary for almost every cardiomyocyte

The down side of this process is that the hearts is very vulnerable to decreased blood flow

During a heart attack you get a blockage in one of more of these vessels which stops the blood flow which stops the oxygen. This is called ischemia

PHSL 232 (30 decks)

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