HRR: excitaation-contraction coupling

Question 1

In what phase of cardiac myocytes AP are calcium channels activated?

Answer 1

Phase 2 (plateau)

Question 2

Name the main ion at each phase of an AP in a cardiac myocyte.

Answer 2

Phase 0: sodium
Phase 1: Cl- and K+
Phase 2: calcium
Phase 3: potassium
Phase 4: potassium

Question 3

What are T tubules?

Answer 3

Continuations of the cell membrane that extend into and through the cell; they act like tunnels through the myocyte.

Question 4

What structure is associated with T tubules?

Answer 4

The sarcoplasmic reticulum.

Question 5

What is DHPR?

Answer 5

An L-type calcium channel in the sarcolemma.

Question 6

What is RYR1?

Answer 6

A structure on the SR that releases calcium.

Question 7

What is SERCA?

Answer 7

Structure on the SR that acts as an ATPase; it burns ATP to bring calcium into the SR.

Question 8

What is phospholamban?

Answer 8

It inhibits SERCA; if we phosphorylate it, the inhibitory effect stops.

Question 9

What are the thin filaments in cardiac myocytes?

Answer 9

Actin, troponin, and tropomyosin.

Question 10

What thin filaments are unique to cardiac myocytes?

Answer 10

Troponin-I, troponin-C, and troponin-T.

Question 11

In what instance would we see Troponin-I, troponin-C, and troponin-T in the bloodstream?

Answer 11

If a cardiac myocyte dies; think MI!

Question 12

What is required to break actin-myosin bridges?

Answer 12

ATP.

Question 13

Compared to skeletal muscle, is myosin in cardiac muscle a slow or fast twitch?

Answer 13

Slow.

Question 14

Describe the steps of excitation leading to calcium release.

Answer 14

1. An AP occurs
2. The inside of a cardiac myocyte becomes positive
3. During phase 2 of the AP, calcium enters the cell
4. This calcium binds RYR on the SR, causing it to release calcium into the cytosol.

Question 15

How is calcium re-sequestered?

Answer 15

SERCA, calcium pump on sarcolemma, and activation of phospholamban.

Question 16

What happens with calcium/the heart if HR increases?

Answer 16

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.

Question 17

What elements can PKA phosphorylate upon beta adrenergic stimulation?

Answer 17

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.

Question 18

At what phase of an AP is there peak contraction?

Answer 18

About the same time as calcium channels close, at the end of phase 2.

Question 19

During how much of contraction is the cell in absolute refractory?

Answer 19

Pretty much all of it!

Question 20

Why can cardiac muscle not be tetanized?

Answer 20

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.

Question 21

What is the sarcomere length-tension relationship?

Answer 21

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.

Question 22

What is the basis for the frank-starling law?

Answer 22

The length-tension relationship.

Question 23

What do we use as an index of stretch on myocytes?

Answer 23

Preload; this explains why increased preload increases output (frank-starling).

Question 24

What is inotropy?

Answer 24

Being able to increase the force of mechanical contraction.

Question 25

How is inotropy associated with increased contraction?

Answer 25

It is associated with being able to make more calcium available to myocytes, which will increase contraction.