Cardiac Muscle Mechanisms Flashcards
how is cardiac muscle structurally similar to skeletal muscles?
sarcomere organization (and therefore striation), and multinucleation (although fewer than skeletal muscle)
what structural differences exist between cardiac and smooth muscle?
intercalacted discs forming a functional syncytium and branching of the cells
what connections is an intercalated disc comprised of? what are their functions?
desmosomes structurally stabilize adjacent cells
gap junctions stabilize structure but also allow electrical connection between two muscle cells
where are T tubules in cardiac muscle cells and how do they differ from their role in skeletal muscle?
they invaginate at the Z line and they carry action potentials but are not coupled with the SR as a triad
what type of metabolism does cardiac muscle employ? what implication does this have for the cell?
aerobic metabolism
abundant myoglobin, glycogen, lipids and mitochondria
what does the action potential cause in a cardiac muscle ceell?
extracellular and SR calcium influx
how is the ryanodine receptor opening different in cardiac muscle than in skeletal muscle?
it is not attached to the L type calcium channel but uses calcium induced calcium release to open the receptor
what are the phases of cardiac action potential?
phase 0: Na current; phase 1: transient outward current; phase 2: Ca current in K current out; phase 3: K current out; phase 4: no net current/rest
what are the important differences between the cardiac and skeletal action potentials?
the cardiac potential is much longer
the action potential is calcium dependant
what causes phase 1, the transient outward current/repolarization of the cardiac muscle cell?
closing of NA channels and the brief activation of a transient outward current
what causes the extension of the refractory period in the cardiomyocyte and what impact does it have on contraction?
it is caused by the slow influx of Ca ions that prevents the cell from repolarizing quickly
it prevents summation of muscle twitches
how do cardiac action potentials propagate?
through gap junctions between cells
positive charge is displaced through the gap junction to depolarize the next cell
how is excitation of cardiomyocytes coupled to calcium release?
during the plateau phase of the action potential, Ca enters from L type Ca channels. These bind to high affinity sites of the ryanodine receptors in the SR and opens them
what percentage of intracellular Ca is contributed from the SR and what percentage from extracellularly in cardiac muscle?
20% extracellular
80% SR
what mechanism is Ca released from the SR in cardiomyocytes?
calcium induced calcium release
what does the sodium calcium exchanger (NCX) do?
exchanges 3 sodium for 1 calcium. can work in either direction into or out of the cell during contraction or relaxation
what are two calcium influx related differences exist between skeletal and cardiac muscle?
cardiac muscle does not couple L type Ca channels and Ryanodine receptors
external calcium contributes to contraction unlike in skeletal muscle
what inactivates ryanodine receptors?
when calcium is at very high concentrations in the cell, it binds to the low affinity site on the ryanodine receptor causing it to close
what are the calcium clearance systems?
SERCA pumps Ca into the SR
NCX exchanges 3Na in and 1Ca out
the plasma membrane Ca ATPase pumps Ca out of the cell
which calcium clearance systems contribute most to calcium removal?
SERCA and NCX
what are the implications of the contribution of extracellular calcium to the cardiac contraction?
cardiac muscle is much more sensitive than skeletal muscle to extracellular calcium levels and is much more sensitive to L type Ca channel blockers
how is calcium released along the SR in cardiomyocytes if it is not coupled with the T tubule?
at the location of the T tubule, there is voltage gated Ca influx into the cell. this is the trigger that opens the ryanodine receptors close to it. the influx of Ca triggers the neighboring ryanodine receptors
once there is Ca influx into the cardiomyocyte, how does this contribute to contraction?
it associates with troponin C and therefore removes tropomyosin from actin’s myosin binding sites
what is the refractory period for a cardiomyocyte action potential?
300 msec
how is contraction of the ventricles and atria separated?
there are two functional syncytia one for the atria and one for the ventricles
what mechanism that is used to increase the force of contraction in skeletal muscle cannot be used in cardiac muscle?
recruitment- all muscle cells already contract because of the gap junctions
what two changes can affect the tension in cardiac muscle?
if the CA is altered or the calcium sensitivity of the myofilaments is altered (changing initial length)
what molecular effect does the ANS have on the heart rate?
changes K conductances in the SA node
what does the frank-starling law of the heart explain?
the increase in cardiac muscle tension without the increase in intracellular calcium levels
what is the frank-starling law?
increased stretching of the ventricle during diastole creates in an increase of contractile force of the chamber
what is the cause for the increase in contractile force when there is already a maximum overlap of myosin and actin in the sarcomere during the frank- sterling law?
sensitivity to Ca is increased because the affinity of troponin C to Ca is increased
what length of myocytes produces the maximal force in the heart?
2.2 micrometers
what are the effects of reater initial length on cardiac muscle function?
increased velocity of contraction, increased shortening, increased work and increased power and increase in maximal tension
what are the two reasons for tension to decrease in muscle cells?
overlapping of actin filaments and stretching of the muscle too far for myosin and actin to have many interactions
how does norepinephrine increase tension development during cardiac twitch?
increases the amount of calcium by g- coupled increase of cAMP and PKA
increases contractility
what changes immediately with administration of NE and what is a more delayed effect?
action potentials are increased immediately and increase in contractility
tension increases eventually with an increase in intracellular calcium concentration that takes longer to occur (in 8 beats)
how does norepinephrine change a cardiac muscle twitch? why does this occur?
it increases tension and decreases duration
pumps blood harder and increases the availability for increased heart rate
what are the two effects of increased cAMP brought about by NE stimulation of beta adrenergic receptors in cardiomyocytes?
increases Ca release by the SR
activation of a protein kinase that phosphorylates phoshpholamban
what is the function of phospholamban?
a regulatory protein that increases the sensitivity of the SERCA and therefore reduces the duration of muscle contraction
what does a positive inotropic agent do to the length-tension curve?
causes an upward shift to increase tension at a particular length (at each length)
what happens to isotonic contractions with inotropic agents?
it increases the length of contraction for a particular tension (lifts a weight farther)
