SM 112a - Cardiac Muscle Contraction Flashcards
The intracellular concentration of which ion is most important in determining contractility?
Ca2+
What is lusitropy?
Myocardial relaxation
Which structure is labeled by #8?

M Line

Which section is labeled by #2?

A band

Which structure is labeled by #9?
Which molecules make up this structure?

Thick filament
Made from myosin light and heavy chains

What is the effect of afterload on the strength of cardiac contraction?
Why?
Afterload decreases the velocity of contraction, which decreases the strength of contraction

What is digoxin?
How does it work?
Digoxin is a drug prescribed to patients with heart failure to increase cardiac output
- It blocks the membrane Na+/K+ ATPase
- Per ATP: 3 Na+ out, 2 K+ in
- If the ATPase cannot pump Na+ out of the cell, intracellular Na+ increases
- Increased Na+ decreases the activity the Na+/Ca2+ exchanger
- Normallly pumps Na+ in and Ca2+ out
- Less Ca2+ out = increased intracellular Ca2+ concentration
- Increased inotropy -> Stronger heart contractions
Note: Digoxin can also slow the HR
Does systolic blood pressure approximate preload or afterload?
Afterload
We are measuring how hard the heart must work to overcome the pressure in the aorta
Describe the troponin complex
The troponin complex is attached to tropomyosin
It is made up of…
- Troponin T (TnT), which binds to tropomyosin
- Troponin C (TnC), which binds to Ca2+
- Troponin I (TnI), which inhibits contraction when it is bound to actin
- It covers up the myosin binding site on actin
If systolic blood pressure increases, what happens to the volume of blood ejected from the heart?
The volume decreases
Increased systolic blood pressure -> slower velocity of contraction -> decreased strength of contraction -> less blood ejected
How would inhibiting cardiac K+ channels affect the cardiac action potential?
Inhibiting cardiac K+ channels would lengthen the cardiac action potential, because it woud take longer for K+ to leave the cell and repolarize the membrane
Why is an increase in intracellular calcium necessary for cardiomyocyte contraction?
Ca2+ must bind to Troponin C in the Troponin complex in order for the tropomyosin + troponin complex to swing out of the way and expose the myosin binding site
The myosin binding site must interact with actin for cross bridge cycling and contraction to occur
Which structure is labeled by #5?

T Tubule

What is the sarcolemma?
The tubular sheath which envelops skeletal and cardiac muscle fibers
It basically acts as the extracellular membrane

Which ion is most responsible for phase 3?

K+
K+ rushes out of the cell (IK1), taking the positive charge with it
This allows the membrane to repolarize

List 3 things that regulate contractility in cardiomyocytes
(All have an effect on Ca2+ concentration in the cytosol)
- Andrenergic signaling acts on B1 receptors in the heart. B1 activation = increased contractility
- Digoxin = increased contractility
-
Heart rate
- Increased HR = increased contractility (Ascending staircase effect aka Bowditch effect aka Treppe)
- Postextrasystolic potentiation: increased contractility of the beat after the extra heart beat
A patient recieves a blood transfusion.
Would you expect the strength of their cardiac contractions to increase or decrease?
Why?
Increase
More blood will increase preload, becaues it will cause the ventricles to fill more during diastole
Increasing preload increases the strength of cardiac contraction
Describe the configuration of actin and myosin in the attached state of cross-bridge cycling
The myosin head is attached to the thin filament after the previous power stroke completion

What is the main mediator of cardiomyocyte relaxation?
The SERCA Pump
(SERCA = Sarcoendoplasmic reticulum Ca2+ ATPase)
How would inhibiting cardiac Ca+ channels affect the cardiac action potential?
Inhibiting cardiac Ca+ channels would prevent Ca2+ from entering the cell. There would be less Ca2+ to oppose the K+ currents, and repolarization would occur more quickly
What is Ca2+ induced Ca2+ release?
How does it work? Describe the steps
The mechanism for excitation-contraction coupling; this is responsible for muscle contraction in response to recieving an action potential
- When the myocyte recieves an action potential, Ca2+ rushes into the myocyte though L-type Ca2+ channels
- Ryanodine receptors (RyR) in the terminal cisternae of the sarcoplasmic reticulum (SR) sense the small increase in cytoplasmic [Ca2+] (trigger Ca2+) and stimulate Ca2+ release from the SR through the RyR
- Ca2+ from the SR causes a x10 to x100 increase in intracellular calcium concentration
- Ca2+ binds to Troponin-C on the thin filament of the sarcomere
- Cross-bridge cycling ensues
What is the ascending staircase effect?
How does it impact cardiac contractility?
Ascending staircase effect = Bowditch effect = Treppe
- Increasing heart rate ->
- Increase in intracellular Ca2+ in SR ->
- Increase in contractility
- More is released when RyRs are activated

Without sufficient ATP, in which step of cross-bridge cycling is the sarcomere arrested?
The attached state
If ATP cannot bind to the actin/myosin complex, the myosin head cannot be released from actin, and it cannot get to the released state.
(It will not be able to release and move to the next actin monomer, 2 positions over)
What is inotropy?
Contractility

























