Excitation/Contraction Coupling Flashcards Preview

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Flashcards in Excitation/Contraction Coupling Deck (35)
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key features of cardiac muscle

large T-tubules

cell to cell electrical connections (gap junctions)

sympathetic fibers to muscle

parasympathetic fibers to muscle

sarcoplasmic reticulum


thin filament


troponin (TnT, TnC, TnI)



thick filament

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



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



binds to tropomyosin



binds to calcium



binds to actin, inhibits contraction



essential, may inhibit contraction



regulatory, may enhance contraction


myocin binding protein C

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



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


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

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


calcium triggered calcium release

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


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

across the sarcolemma and transverse tubules


What happens to calcium during relaxation of heart muscle?

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


effect of sympathetic stimulation on the heart

increases heart rate and the slow inward calcium current

increases calcium release and increases contractility

speeds calcium reuptake process


Descrive the excitation-contraction coupling in cardiac muscle

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


cardiac glycosides

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


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

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


T-type calcium channel

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


L-type calcium channel

long-lasting, large

open at less negative voltage (-40 mV)

inactivate slowly

affected by calcium antagonists

found throughout the myocardium

affected by beta-agonists


dihydropyridine receptor (DHP)

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


ryanodine receptor (RyR)

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

physically connected to the DHPR in skeletal muscle


calcium handling in the myocardium

75% back into the SR

25% Na-Ca exchanger

1% through sarcolemmal calcium pump and mitochondrial calcium pump



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


cAMP-dependent PKA

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


calsequestrin and calreticulin

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


other proteins that bind Ca++ in the SR

histidine-rich calcium binding protein and sarcalumenin

sarcalumenin regulates Ca++ pump activity


Describe the crossbridge cycle.

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


beta-receptor effects

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