HRR: excitaation-contraction coupling Flashcards
In what phase of cardiac myocytes AP are calcium channels activated?
Phase 2 (plateau)
Name the main ion at each phase of an AP in a cardiac myocyte.
Phase 0: sodium
Phase 1: Cl- and K+
Phase 2: calcium
Phase 3: potassium
Phase 4: potassium
What are T tubules?
Continuations of the cell membrane that extend into and through the cell; they act like tunnels through the myocyte.
What structure is associated with T tubules?
The sarcoplasmic reticulum.
What is DHPR?
An L-type calcium channel in the sarcolemma.
What is RYR1?
A structure on the SR that releases calcium.
What is SERCA?
Structure on the SR that acts as an ATPase; it burns ATP to bring calcium into the SR.
What is phospholamban?
It inhibits SERCA; if we phosphorylate it, the inhibitory effect stops.
What are the thin filaments in cardiac myocytes?
Actin, troponin, and tropomyosin.
What thin filaments are unique to cardiac myocytes?
Troponin-I, troponin-C, and troponin-T.
In what instance would we see Troponin-I, troponin-C, and troponin-T in the bloodstream?
If a cardiac myocyte dies; think MI!
What is required to break actin-myosin bridges?
ATP.
Compared to skeletal muscle, is myosin in cardiac muscle a slow or fast twitch?
Slow.
Describe the steps of excitation leading to calcium release.
- An AP occurs
- The inside of a cardiac myocyte becomes positive
- During phase 2 of the AP, calcium enters the cell
- This calcium binds RYR on the SR, causing it to release calcium into the cytosol.
How is calcium re-sequestered?
SERCA, calcium pump on sarcolemma, and activation of phospholamban.
What happens with calcium/the heart if HR increases?
There is not enough time to properly clear calcium, causing it to build up in the cell. This causes the cell to remain slightly contracted and makes the cell stiffer.
What elements can PKA phosphorylate upon beta adrenergic stimulation?
Phospholamban, sodium-potassium pump, L-type calcium channels, and RYR (calcium release channels). All of this will allow for faster sequestering of calcium to be ready for the next strong contraction.
At what phase of an AP is there peak contraction?
About the same time as calcium channels close, at the end of phase 2.
During how much of contraction is the cell in absolute refractory?
Pretty much all of it!
Why can cardiac muscle not be tetanized?
The effective refractory period remains for pretty much the entirety of contraction. As a result, another impulse doesn’t cause contraction while another contraction is still occurring. One impulse, one contraction.
What is the sarcomere length-tension relationship?
There is an optimal level of tension/length in a sarcomere that allows for optimal contraction; the myocyte does not allow the sarcomere to stretch beyond this point because that would be bad. Up to a point, the more we pull out the length the better the contraction.
What is the basis for the frank-starling law?
The length-tension relationship.
What do we use as an index of stretch on myocytes?
Preload; this explains why increased preload increases output (frank-starling).
What is inotropy?
Being able to increase the force of mechanical contraction.
How is inotropy associated with increased contraction?
It is associated with being able to make more calcium available to myocytes, which will increase contraction.
