Cardiac muscle Flashcards
(37 cards)
What appearance properties does a cardiac myocyte share with skeletal muscle?
- Multinucleated cells
- Sarcomeres with A and I bands and a Z line
How does a cardiac myocyte differ in appearance from a skeletal muscle cell?
- Myocytes are branched
- Intercalated discs separate adjacent myocytes (with gap junctions and desmosomes)
- T-tubules only invaginate at the Z-line
The cardiac action potential has a ______ phase, creating a ______ absolute refractory period. It is also _____-dependent.
Plateau; long; Calcium
Why do cardiac myocytes have gap junctions? Described what happens here
To allow action potentials to propagate quickly and to contract as two organized syncytia. If a neighboring cardiac myocyte was stimulated to produce an action potential, some positive charge can move into a cell and depolarize its membrane, opening voltage gated Na+ channels and starting an action potential there.
How do calcium levels rise in a cardiac myocyte?
Some calcium enters the sarcoplasm via L-type calcium channels. This calcium binds to high affinity sites on Ryanodine receptors on the SR, causing massive release of Ca2+ (most impt mech). The NCX exchanger may also work in reverse to bring Ca2+ into a cell.
How does a cardiac myocyte clear Ca2+ from its sarcoplasm?
SERCA pumps ATP back into the SR (most impt mech). Also PMCA pumps Ca2+ outside of the cell and the NCX uses the Na+ gradient to push 1 Ca2+ out of the cell while letting 3 Na+ in.
What happens when Ca2+ binds the high affinity site on the Ryanodine receptor? The low affinity site?
High affinity- Ryanodine receptor releases Ca2+ from the SR (Calcium-induced Ca2+ release) which propagates down along the SR
Low affinity- Ryanodine closes and stops releasing Ca2+
How does Ca2+ regulate contraction? Is this more similar to skeletal muscle or smooth muscle regulation?
It binds to Troponin C which moves tropomyosin off of actin.
Skeletal muscle
Does the heart contract by twitch? Tetanus/summation? Does recruitment occur?
The heart can only contract by twitch. The long absolute refractory period prevents summation and tetanus. It does not recruit other motor units.
What does the Frank-Starling law of the heart say?
The ventricle will pump whatever amount of blood you put into it. An increase in EDV (and thus in length and tension) corresponds to an increase in SV
What happens to Po (maximum load) if a cardiac myocyte is stretched? What about shortening (change in length)? Work? Power?
Increased length increases maximum load and distance of shortening. Thus it also increases work and power
Why does tension increase in heart muscle cells with increasing length even when thick and thin filaments have maximal overlap?
The increased stretch increases the sensitivity of the muscle. Troponin C is better able to bind Ca2+ when it’s more stretched out thus it is more likely to move off of actin and allow contraction.
How does norepinephrine increase tension in a cardiac myocyte?
Norepi binds B1 adrenergic receptor, stimulating an increase in cAMP, activating PKA and increasing calcium release. This increases tension in the cell (and is an increase in contractility)
What effect does norepi administration have on the duration of a twitch? Why?
It decreases duration. It inactivates phospholamban which acts as a brake on SERCA. Thus, Ca2+ can be cleared more effectively.
How long does it take for an AP to change after norepi administration? For an increase in tension?
AP- immediately
Tension- about 8 heartbeats
On a Ca2+- tension curve, what effect does increased sensitivity have? What effect does increased contractility have?
Increased sensitivity shifts the curve up b/c more tension is created at the same Ca2+ level. Increased contractility shifts the curve up along the curve b/c more Ca2+ is released
On a length-tension curve, what effect does increased contractility have?
It shifts the curve up. At any length, the muscle can produce more tension b/c it has greater Ca2+ levels in its sarcoplasm
What happens to Po (maximum load) if a cardiac myocyte experiences an increase in contractility? What about shortening (change in length)? Work? Power?
Po and shortening increase b/c the length-tension curve is shifted up. Thus, work and power also increase
In skeletal muscle, work = _______ x __________. In cardiac muscle, work= ________ x __________. Thus, ______ is analogous to _______ and ______ is analogous to _______.
Skeletal muscle: W= force (tension) x change in length
Cardiac muscle W= pressure x change in volume
Force is analogous to pressure; length is analogous to volume
When (in terms of pressure) will the LV fill? When will it empty?
It will fill when P(atrium) > P(ventricle)
It will empty when P(ventricle) > P(aorta)
What occurs when the mitral valve is open? When it is closed and the aortic valve is closed? What happens when the aortic valve is open? What about when it and the mitral valve are both closed
Mitral valve open- ventricle fills
-> isovolumic contraction
Aortic valve open- ventricle empties
-> isovolumic relaxation
What can you say about P (atrium) and P (ventricle) when the mitral valve closes? How about P (aorta) and P (ventricle) when the aortic valve closes?
Mitral valve close: P(atrium) = P(ventricle)
Aortic valve close: P(ventricle)= P aorta
What does the end-systolic pressure volume relationship (ESPVR) curve tell us about the the cardiac cycle? Can this curve change? If so, how?
It defines the maximal pressure that can be generated by the LV at any given volume.
It can shift. Norepi administration shifts the curve to the L, allowing the ventricle to fill with more blood, increasing contractility.
What is compliance- both mathematically and in words?
How easy something is to fill. C= change in volume/ change in pressure
