Physiology for MRCEM Primary

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Cardiovascular physiology

Excitation contraction coupling

[box type=”download”]  Fundamental role of calcium and its origin in sarcoplasmic reticulum  Sequestration of calcium via Ca-ATPase and sodium/ calcium exchange pumps  Biochemical basis of the Treppe effect [/box]


Cardiac muscle contracts when intracellular Ca2+ rises above 100 nM.
The Ca2+ entry during the AP accounts only for ∼25% of the rise in intracellular Ca2+.
The rest is released from the sarcoplasmic reticulum (SR).
APs travel down invaginations of the sarcolemma called T-tubules.
Ca2+ entering the cell during the AP plateau activates Ca2+-sensitive Ca2+ release channels (ryanodine receptors, RyR) in the SR, allowing stored Ca2+ to flood into the cytosol; this is Ca2+-induced Ca2+ release (CICR).
Peak intracellular [Ca2+] normally rises to ∼2 μM, although maximum contraction occurs above 10 μM.


Ca2+ is removed from cytosol into the SR (sequestered) by the sarco/endoplasmic reticulum Ca2+ ATPase (SERCA).
Ca2+ that entered during the AP will be removed by the Na+–Ca2+ exchanger (NCX) in the membrane, which pumps one Ca2+ ion out in exchange for three Na+ ions, using the Na+ electrochemical gradient as an energy source.
This is relatively slow, and continues during diastole.
If the diastole is shortened, i.e. when the heart rate rises, more Ca2+ is left inside the cell and the cardiac force increases.
This is the staircase or Treppe effect.