Flashcards in cardiac muscle structures 3 Deck (31):
1. allows the sarcomere to change
2. the major protein allowing for movement
3. acts like an elastic spring
4. One of the major proteins responsible for passive elastic properties of the cell (and thus for diastolic properties of the heart)
more rigid, increases stiffness
can be short term phosphorylated
Titin regulation sites
there are a ton of them
steps of muscle contraction
1. Action potential leads to calcium release.
2. Calcium binds to troponin C.
3. Troponin complex undergoes structural change, moving tropomyosin out of the way.
4. Myosin binds actin and crossbridge moves.
5. Calcium is released, tropomyosin reblocks binding site - relaxation
Frank-Starling Law of the Heart
The effect of increasing preload on force of contraction:
the greater the volume of blood entering the heart during diastole (end-diastolic volume), the greater the volume of blood ejected during systolic contraction (stroke volume) and vice versa.
The Frank-Starling law of the heart describes the effect of .
increasing preload on the force of contraction.
the greater the volume of blood entering the heart during diastole, the greater the volume of blood ejected during contraction.
the frank starling law is due to
thelength-tension relationship described – as we increase the fiber length, the force of contraction for a given stimulus is increased
When cardiac muscle is stimulated to contract at low resting lengths, the amount of active tension developed is ____.
When you increase the muscle length, the active tension developed ____
Frank-Starling’s law of the heart: myofilament length-dependent activation
“The Greater the Preload, the greater the force generated”
Mechanisms behind the length-tension relationship
1. extent of the overlap
2. change in the sensitivity of the myofilament to calcium
3. increased calcium release
Extent of overlap:
Histological studies indicate that the changes in the resting length of the whole muscle are associated with proportional changes in the individual sarcomere. Peak tension development occurs at sarcomere lengths of 2.2 to 2.3 mM.
Change in the sensitivity of the myofilament to calcium:
At short lengths only a fraction of the potential cross-bridges are activated by a given increase in calcium. At longer lengths, more of the cross-bridges become activated by the same change in intracellular calcium. No time delay in the “sensor”.
Increased calcium release:
Occurs several minutes after changing the length of the muscle. May be due to stretch-sensitive ion channels in the cell membrane.
Calcium Sensitivity of Cardiac Muscle
1. Calcium is the central factor in myocardial contraction
2. The responsiveness of the myofilament to calcium is “calcium sensitivity”
factors that regulate calcium sensitivity of the myofilament
1. TnI phosphorylation
2. Isoform composition
3. sarcomere length
the pressure that ventricle has to generate in order to eject blood out of the chamber – most closely related to aortic pressure (except with disease)
what changes the velocity on the sarcomeric level?
1. Phosphorylation of MLC
2. Phosphorylation of MyBPC
THE LAW OF LAPLACE
T = P x r/h
Excitation of cardiac myocytes initiates contraction by
increasing the cytosolic calcium that activates the contractile proteins by binding to troponin, moving tropomyosin and allowing myosin binding to actin.
The mechanical response of the myocyte depends on
3. the contractility of the myofilament
the initial length of the myocyte
the tension that needs to be developed
the contractility of the myofilament is determined mainly by
The cardiac myocyte length-tension relationships are correlated with
changes in pressure-volume in the intact ventricle.
Changes (both translationally and post-translationally) of the myofilament proteins are associated with
Proteomic regulation of crossbridge cycling underlies:
changes in contraction/relaxation of the heart with exercise, age, disease, etc
Thin and thick filaments contain
regulatory proteins that are modifiable