Cardiac Excitation-Contraction Coupling & Energy Utilization Flashcards
Differences Between Structure of Cardiac and Skeletal Muscle
- contractile filaments are nearly identical
- eg. troponin complex is different, used as indicator of severe of MI
- SR is smaller, particularly coupling regions and dyads
- t-tubules are larger in diameter and penetrate at Z discs
- mostly dyads, few triads, where excitation contraction coupling originates
- 40% of cell volume occupied by mitochondria - huge reliance on aerobic metabolism
- often see glycogen granules and lipid droplets in cardiac muscle
Excitation-Contraction Coupling in Cardiac Muscle
- after depolarization occurs, calcium enters myocardial cells through voltage gated calcium channels
- calcium from EC is not enough to cause strong enough myocardial contraction to maintain cardiac output
- ryanodine receptors in SR not physically coupled to voltage gated calcium channels
- RYR located in SR directly opposite VG calcium channels in t tubules
- RYR are sensitive to rises in calcium concentration in myoplasm
- calcium concentration in dyadic space btwn SR and t tubules rises to micromolar range from EC calcium, causing RYR to open and release large amounts of SR calcium
- myoplasmic calcium reaches micromolar range with calcium from SR, allowing full myocardial contraction
Calcium Induced Calcium Release
-small amounts of calcium from EC space are able to cause RYR to open releasing large amounts of calcium from SR
Return to normal of calcium concentrations
- amount of calcium that is brought in through voltage gated calcium channels is moved out of cell by sodium calcium exchanger (NCX)
- amount of calcium released through RYR from SR is returned to SR by SERCA
NCX
Sodium Calcium Exchanger
- brings 3 sodiums in for 1 calcium out
- throughout sarcolemma
- more efficient than SERCA
Myocardial Cell Without EC Calcium
- it will not contract
- contrast to skeletal muscle
Phospholamban
- coupled to SERCA
- regulates how quickly SERCA moves calcium back into SR
- when coupled - “brakes” SERCA
Calsequestrin
- coupled to RYR2 in SR
- stores calcium in SR
Heart Failure and Dyadic Space
- in HF, space between SR and t tubule starts to increase
- get down regulation of proteins
Resting HR
- SR is not releasing full amounts of calcium, maintained at low level
- no saturation of troponin G
Beta 1 adrenergic stimulation
- positive chronotropic effect (increasing heart rate)
- positive ionotropic effect (increasing force of contraction)
- positive lusitropic effect (increasing rate of relaxation)
- regulated through protein kinase A which phosphorylates proteins that regulate myoplasmic calcium concentrations
- going to learn about effects of phosphorylation in later cards
Positive Lusitropic Effect
- reduces amount of time ventricles stay in systole
- maintains period of diastole with increasing HR
- diastole important for filling of ventricles and allowing perfusion of blood through coronary capillaries
Phosphorylation of Voltage Gated Calcium Channels
-increases open probability of channel, allowing more calcium to enter cell with each heartbeat
Phosphorylation of Phospholamban
- causes it to move away from SERCA
- brake no longer applied to SERCA
- rate at which SERCA moves calcium into SR increases
With phosphorylation of phospholamban and VG calcium channels, what happens?
- more calcium moving into cell from EC space
- more calcium moving into SR
- therefore, more calcium available for RYR to pump out
- increases force of contraction and rate of force development
