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Influx of sodium ions
1%
2/297
Efflux of potassium ions
39%
115/297
Influx of calcium ions from the sacroplasmic reticulum
4%
13/297
Influx of calcium ions from outside the myocyte
3/297
Efflux of calcium ions
53%
156/297
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Cardiac muscle relaxation occurs when intracellular Ca2+ levels return to baseline. Since Ca2+ enters the cytoplasm to trigger contraction, it must then leave the cytoplasm to return to baseline. After the myocyte is depolarized, L-type Ca2+ channels (long-acting, voltage gated, active in Phase 2 of the action potential) open to allow Ca2+ to enter the cell, which leads to calcium-induced-calcium-release (CICR) via the ryanodine receptor (ligand gated, active in Phase 2 as well), a phenomenon unique to cardiac myocytes (compared to skeletal muscle). Eventually, intracellular Ca2+ binds troponin, which allows actin and myosin to bind and contract. To relax, Ca2+ leaves the cytoplasm via several mechanisms: 1) the Na+/Ca2+ exchanger, which allows 1 Ca2+ to exit for every 3 Na+ that enter, 2) the Ca2+ ATP-ase pump in the cell membrane, which pumps Ca2+ out of the cell, and 3) the Ca2+ ATP-ase pump in the sarcoplasmic reticulum (SR) membrane, which pumps Ca2+ into the SR. Illustration A shows cardiac muscle under a microscope. Illustration B depicts the channels, ions, and cellular compartments important in excitation contraction coupling. Incorrect answers: Answers 1 & 2: K+ actually must enter the myocyte and Na+ must leave it (via Na+/K+ ATPase) to establish the Na+ gradient that drives the Na+/Ca2+ exchanger. Answers 3 & 4: Ca2+ must enter the cell, first from outside the myocyte, and then from the SR (via CICR) for the cell to contract, but not to relax.
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