Flashcards in Cardiac Muscle Structure and Fxn Deck (19)
What are the specialized (and unique) features of cardiac muscle?
-composed of interconnected mono-nucleated cells embedded in a weave of collagen
-longer repolarization than skeletal muscle (prevents tetanus)
-thin filament contraction (versus smooth muscle which is thick filament regulated)
-mostly composed of myofibril and mitochondria (main fxn is to contract).
T of F? Cardiac muscle is under control of neural input
mostly F. It is autonomic (SA node) but it will still receive input from neurons it is just not necessary
Cardiac cell coupling is both _____ and ______.
mechanical and electrical. These types of communication occur at the gap junctions.
now remember... Cardiac muscle is regulated by what kind of filament?
What is TN-C, TN-I, TN-T, and TM and what is important about each?
-Troponin Calcium- has only one Ca binding site
-Troponin Inhibitory- is highly regulated by phosphorylation (PKA sites)
-Troponin tropomyosin- Has a unique N terminal extension that that is involved in regulation of calcium sensitivity
-Tropomyosin- only alpha isoform (unlike skeletal in which there is both alpha and beta)
What are the basics of the molecular basis of the cross-bridge cycle?
resting muscle- at low intracellular Ca2+ Tn-Tm complex is binding to actin sites and blocking it from binding to myosin. With an increase in myoplasmic Ca2+, TN releases its inhibition (Ca first binds TN-C and then starts moving the other troponins until it moves tropomyosin). Once tropomyosin is moved myosin can bind and undergo power stroke. The myofilaments shorten (sliding filament theory). Then tropomyosin reblocks binding site as calcium is released (relaxation).
What are the two major isoforms of Titin and which one is stiffer?
N2Ba- less stiff
What is the function of Titin?
functions as an elastic spring. largely responsible for resting tension of the cardiac myocyte.
The Stroke volume of the heart ______ in response to an increase in the volume of blood filling the heart.
What is a simpler way of stating this? What law is it?
increase in pre-load leads to increase in stroke volume
Frank Starling Law
The Frank Starling Law can be explained by what relationship? What things can modify this relationship?
1. extent of overlap of the thick and thin filaments- there is a sweet spot of overlap, stretching can make the overlap better for contraction.
2. changes in Ca sensitivity- at longer lengths more cross-bridges are activated by the same amt of calcium (at short lengths not all potential cross bridges are engaged).
3. Increased Ca release- may be due to stretch sensitive ion channels
What are two important ways that Ca sensitivity is regulated?
1. Shorter Tn-T are more Ca sensitive (N-terminal extension of Tn-T decreases Ca sensitivity)
2. PKA phosphorylation of Tn-I decreases Ca sensitivity
What are the three regulators of Stroke volume?
pre-load, afterload, and contractility
With decreased afterload what happens to Ejection fraction (or SV)?
increases. Doesn't have to work as hard to push the blood out so with same amount of force it will push more out.
If you increase afterload what happens to velocity?
What changes velocity on the level of the sarcomere?
What is special about these things?
-phosphorylation of MLC (light chain)
-phosphorylation of MyBPC (myosin binding protein C)
they are thick filaments
Pre-load is ______ mediated while afterload is _____ mediated.
contractility is determined mainly by:
At constant volume an increase in the tension of individual cells in the wall causes an increase in intraventricular ______.