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Cardiovascular > Excitation/Contraction Coupling > Flashcards

Excitation/Contraction Coupling Flashcards

1
Q

key features of cardiac muscle

A

large T-tubules

cell to cell electrical connections (gap junctions)

sympathetic fibers to muscle

parasympathetic fibers to muscle

sarcoplasmic reticulum

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2
Q

thin filament

A

actin

troponin (TnT, TnC, TnI)

tropomyosin

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3
Q

thick filament

A

myosin - heavy chains, 2 sets of light chains (MLC, regulatory and essential), myosin binding protein C

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4
Q

tropomyosin

A

2 alpha-helices that coil and reside in the grooves in the actin, serves to regulate interaction between actin and myosin

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5
Q

TnT

A

binds to tropomyosin

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6
Q

TnC

A

binds to calcium

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7
Q

TnI

A

binds to actin, inhibits contraction

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8
Q

MLC-1

A

essential, may inhibit contraction

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9
Q

MLC-2

A

regulatory, may enhance contraction

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10
Q

myocin binding protein C

A

associated with the S2 subunit of the head - may be involved in cardiomyopathies

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11
Q

titin

A

a giant protein that extends from the Z-line to the center of the thick filament

the portions that lie within the A-band are rigid, while the regions in the I band are more elastic

may play a role in transducing sustained stretch into a growth signal

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12
Q

Describe the conformational change of the light chain in the presence of calcium.

A

calcium binds to troponin C, which unblocks the active sites between actin and myosin, allowing cross-bridge cycling

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13
Q

calcium triggered calcium release

A

the calcium entering the cell during an action potential stimulates the release of an additional amount of calcium from the sarcoplasmic reticulum

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14
Q

From where does calcium enter the cell during an action potential?

A

across the sarcolemma and transverse tubules

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15
Q

What happens to calcium during relaxation of heart muscle?

A

removed from the cytoplasm by re-uptake of calcium into the SR by an energy dependent calcium pump

extruded from the cell to the interstitial fluid by an electrically neutral exchange for sodium

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16
Q

effect of sympathetic stimulation on the heart

A

increases heart rate and the slow inward calcium current

increases calcium release and increases contractility

speeds calcium reuptake process

17
Q

Descrive the excitation-contraction coupling in cardiac muscle

A
  1. Action potential travels along surface and down T-tubes
  2. T-tube depolarization triggers SR to release Ca++ into cytoplasm of cell
  3. Ca++ binds to the contractile apparatus (Troponin C)
  4. Ca++ binding activates contractile apparatus and cell contracts
  5. Contractile apparatus is active as long as Ca++ is remains elevated
  6. The Ca++ in the cytoplasm is removed by SR Ca++ pumps and Na-Ca exchange
  7. Cell relaxes as Ca++ is cleared from cytoplasm
18
Q

cardiac glycosides

A

inhibit Na-K pump, which results in intracellular Na+ accumulation

19
Q

calcium influx as a trigger for SR calcium release in cardiac muscle

A
  1. T-tube depolarization triggers a small Ca++ influx through the DHP (dihydropyridine) receptor Ca++ channel
  2. This trigger Ca++ signal binds to the SR Ca++ release channel (i.e. the ryanodine receptor).
  3. Ca++ binding caused RyR to open and Ca++ is released from the SR
  4. This process is called Ca++ -induced Ca++ release
20
Q

T-type calcium channel

A

transient, tiny

open at more negative voltage (-50 to -60 mV)

short bursts of opening

do not interact with calcium antagonists

primarily found in atrial tissue

not affected by beta-agonists

21
Q

L-type calcium channel

A

long-lasting, large

open at less negative voltage (-40 mV)

inactivate slowly

affected by calcium antagonists

found throughout the myocardium

affected by beta-agonists

22
Q

dihydropyridine receptor (DHP)

A

a specialized calcium channel (L-type) in the T-tubule membrane

23
Q

ryanodine receptor (RyR)

A

forms “foot” structure and is the SR calcium release channel in cardiac muscle

physically connected to the DHPR in skeletal muscle

24
Q

calcium handling in the myocardium

A

75% back into the SR

25% Na-Ca exchanger

1% through sarcolemmal calcium pump and mitochondrial calcium pump

25
Q

phospholamban

A

normally inhibits SR calcium pump (SERCA-2)

when phosphorylated by cAMP-dependent PKA, its ability to inhibit the SR calcium pump is lost, allowing the pump to actively pull Ca++ into the SR

26
Q

cAMP-dependent PKA

A

any substance that activates this kinase will decrease inhibition of the SR Ca++ pump through phospholamban phosphorylation

agents such as epinephrine, norepinephrine, and beta-agonists do this

this accelerates Ca++ uptake into the SR, which produces myocardial relaxation

27
Q

calsequestrin and calreticulin

A

proteins that bind Ca++ in the SR

in cardiac muscle, calsequestrin is dominant

both have about 50 Ca++ binding sites per protein molecule

calsequestrin and histidine-rich calcium binding protein regulate Ca++ release

28
Q

other proteins that bind Ca++ in the SR

A

histidine-rich calcium binding protein and sarcalumenin

sarcalumenin regulates Ca++ pump activity

29
Q

Describe the crossbridge cycle.

A

ATP binds to myosin head, cuasing dissociation of the actin-myosin complex

ATP is hydrolyzed, causing myosin heads to return to their resting conformation

a cross-bridge forms and the myosin head binds to a new position on the actin

phosphate is released and myosin heads change conformation, resulting in the power stroke and the filaments slide past each other

ADP is released, resetting the cycle

30
Q

beta-receptor effects

A

activation results in the phosphorylation of phospholamban and Tn-I

increases the rate of relaxation.direct impact on ventricular filling and coronary perfusion - lusotropic effect

increases the movement of calcium into the myocardium - ionotropic effect

31
Q

dromatropy

A

increases in conduction

32
Q

chronotropy

A

increases in heart rate

33
Q

ascending staircase (treppe)

A

with increasing frequency of contraction, there is less time for calcium to be removed from the cell

the cell accumulates calcium, resulting in more forceful contractions

causes increased number of depolarizations per minute and slower inactivation of current

34
Q

rest potentiation

A

pause in repetitive contractions permits calcium stores to return to a releaseable form

contraction after the pause is augmented

35
Q

post-extrasystolic potentiation (PESP)

A

premature contraction results in less calcium to release from SR

the poxt-extrasystolic beat is greater because of the increased calcium into the cells

Cardiovascular (46 decks)

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