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Cardiac Muscle Contraction and Relaxation Mechanisms

Learn about the histology of cardiac muscle, role of key proteins, cellular events, ion involvement in contraction, and heart relaxation process. Explore the structure of muscle and factors influencing stroke volume.

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Cardiac Muscle Contraction and Relaxation Mechanisms

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  1. The contraction of the Heart Reverend Dr. David C.M. Taylor School of Medicine dcmt@liverpool.ac.uk http://www.liv.ac.uk/~dcmt

  2. Learning outcomes • By the end of this lecture you should be able to discuss • The histology of cardiac muscle • The role of myosin, actin, troponin and tropomyosin • The importance of calcium for contraction • Starlings law • Cellular and molecular events underlying cardiac contraction and relaxation • The role of Na+, K+ and Ca2+ in cardiac contractility

  3. Structure of muscle Chapter 13 p 147 in Preston and Wilson (2013) Chapter 9 p 437 in Naish and Court (2014)

  4. Histology

  5. The sarcomere Actin filaments Myosin filaments Z line Chapter 12 p 136 in Preston and Wilson (2013) Chapter 9 p 437 in Naish and Court (2014)

  6. In more detail Troponin-tropomyosin complex actin myosin binding site myosin

  7. In the presence of Calcium • Tropomyosin shifts to expose the myosin binding site • Myosin binds to binding site • ATP is used to provide the energy to flex the myosin head • The muscle shortens

  8. The order of events Chapter 13 p 147 in Preston and Wilson (2013) Chapter 9 p 437 in Naish and Court (2014) • The muscle depolarises • Excitation spreads over the sarcolemma and into the T-tubules (there are fewer T-tubules than in skeletal muscle) • L-type Ca2+ channels open (dihidropyridine receptors), increasing sarcoplasmic Ca2+ levels • Ca2+ induces Ca2+ release from the sarcoplasmic reticulum • Ca2+ binds to tropomyosin • Tropomyosin shifts to expose the myosin binding site • Myosin binds to binding site • ATP is used to provide the energy to flex the myosin head • The muscle shortens

  9. Then Chapter 13 p 150 in Preston and Wilson (2013) Chapter 9 p 440 in Naish and Court (2014) The heart does not remain contracted, but relaxes. This is caused by the activity of the SERCA The SERCA is a Sarcoplasmic/Endoplasmic Reticulum Calcium ATPase So energy is used to draw Ca2+ back into the sarcoplasmic reticulum. And the myosin is released from the actin filaments…

  10. Na+, K+ and Ca2+ The principles are exactly the same as for neurones But the action potentials last much longer And Ca2+ ionsare more important Na+ and K+ regulate the rate of contraction Ca2+ regulates the force of contraction The more Ca2+,for whatever reason, the greater the force of contraction All three are regulated by the autonomic nervous system

  11. The action potential (revision) Fully permeable to Na+(+40mV) +40mV Resting membrane potential(-70mV) -55mV -70 mV Fully permeable to K+ (-90mV) 1mS

  12. The action potential (revision) VANC close Fully permeable to Na+(+40mV) +40mV VANC open gNa+ gK+ Resting membrane potential(-70mV) stimulus -55mV -70 mV Fully permeable to K+ (-90mV) 1mS

  13. 0 mV -70 0 mS 300 Pacemaker activity • The rhythm of the pump is provided by the pacemaker activity of some specialized muscle cells in the wall of the right atrium - the sinoatrial node • There is a steady inward current of both Na+ and Ca2+ • Which causes a gradual depolarisation

  14. Factors affecting stroke volume Preload Afterload Contractility

  15. 100 80 60 40 20 Tension developed % 40 60 80 100 120 140 160 Percentage sarcomere length (100% = 2.2 µm) Preload • increased end-diastolic volume stretches the heart • cardiac muscles stretch and contract more forcefully • Frank-Starling Law of the heart

  16. Starling’s Law 2.2 m 3.8 m 1.8 m 100 80 60 40 20 Tension developed % 40 60 80 100 120 140 160 Percentage sarcomere length (100% = 2.2 m)

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