Excitation/Contraction Coupling Flashcards
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
actin
troponin (TnT, TnC, TnI)
tropomyosin
thick filament
myosin - heavy chains, 2 sets of light chains (MLC, regulatory and essential), myosin binding protein C
tropomyosin
2 alpha-helices that coil and reside in the grooves in the actin, serves to regulate interaction between actin and myosin
TnT
binds to tropomyosin
TnC
binds to calcium
TnI
binds to actin, inhibits contraction
MLC-1
essential, may inhibit contraction
MLC-2
regulatory, may enhance contraction
myocin binding protein C
associated with the S2 subunit of the head - may be involved in cardiomyopathies
titin
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
- Action potential travels along surface and down T-tubes
- T-tube depolarization triggers SR to release Ca++ into cytoplasm of cell
- Ca++ binds to the contractile apparatus (Troponin C)
- Ca++ binding activates contractile apparatus and cell contracts
- Contractile apparatus is active as long as Ca++ is remains elevated
- The Ca++ in the cytoplasm is removed by SR Ca++ pumps and Na-Ca exchange
- 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
- T-tube depolarization triggers a small Ca++ influx through the DHP (dihydropyridine) receptor Ca++ channel
- This trigger Ca++ signal binds to the SR Ca++ release channel (i.e. the ryanodine receptor).
- Ca++ binding caused RyR to open and Ca++ is released from the SR
- 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
