DSA: Cardiac Electromechanical Coupling Flashcards
Explain excitation-contraction coupling in cardiac muscle from the depolarization of the T-tubules to Ca2+-troponin C binding
1) Depolarization of T-tubules cause the opening of DHP receptors which cause influx of extracellular Ca2+
2) The increase in intracellular Ca2+ triggers release of more Ca2+ from the SR through Ryanodine receptors
3) Intracellular Ca2+ increases even more and Ca2+ binds troponin C
Describe “Ca2+-induced Ca2+ release
Increased Ca2+ intracellularly through DHP channels trigger the release of more Ca2+ from SR through ryanodine receptors
What is the Ca2+ that enters the cell during the plateau of the AP called?
Trigger Ca2+
What 2 things determine how much Ca2+ is released from the SR of cardiac muscle?
- Amount of Ca2+ previously stored
- Size of inward Ca2+ current during plateau
What does the magnitude of tension during cross bridge cycling of cardiac muscle depend on?
Intracellular Ca2+ concentration
When does relaxation of cardiac muscle occur in terms of excitation-contraction coupling?
- When Ca2+ is reaccumulated in the SR by Ca2+ ATPase (SERCA)
- Ca2+ that entered the cell leaves via Ca2+ ATPase and Ca2+-Na+ exchange
How does the SR of cardiac and skeletal muscle compare?
SR is less extensive in cardiac muscle
How do the T-tubules between cardiac and skeletal muscle compare?
Cardac: T-tubules are along the Zline and form a diad with 1 cisterna
Skeletal: T-tubules are larger (store much more Ca2+!) and at the end of thick filaments forming a triad with 2 cisternae
What is the role of gap junctions in cardiac versus skeletal muscle?
Cardiac: myocytes connected by gap jnxs forming syncitium -> allows rapid coordination of myocyte contraction (AP propogates through intercalated discs -> AP travels through gap jnxs in atria only!)
Describe Starling’s law of the heart?
The greater the heart muscle is stretched during filling, the greater the force of the concentration and the greater the quantity of blood pumped into aorta
Define afterload
Aortic pressure -> increased afterload = increased ventricular pressure = increased SV = increased end systolic volume
Define preload
Tension of the blood pushing out against the walls of the chamber just before it contracts -> AKA venous return or end diastolic volume
What does an increase in preload cause?
Increase in stroke volume
- Increase in preload = increase in venous return and therefore end diastolic volume and therefore SV
How does an increase in preload shift the ventricular pressure-volume loop?
Shifts is to the right, increasing the width of the curve which is equivalent to the stroke volume
What effect does an increase in contractility have on the pressure-volume loop?
Shifts it up and left -> increases width of curve (SV) and ventricular pressure
