Cardio-Physio-Cardiac myocytes Flashcards
What type of junction do connexons form?
gap junctions that allow ions to back and forth allowing heart cells to be connected electrically
Calcium comes from the ECF in cardiac/skeletal muscle?
cardiac muscle
What is the role of calcium in the cardiac cell?
Action potential -L-type calcium channel opened and calcium flows into cell- calcium from ECF binds to channel on sarcoplasmic reticulum which releases its calcium- calcium then acts on sarcomeres
What is calcium-induce calcium release (CICR)?
When calcium ions induce calcium induced channels to release more calcium from sarcomplasmic reticulum in cardiac muscle cell.
Which is the main way by which calcium moves into the cardiac muscle cell cytosol?
From calcium-induced calcium release from the sarcomplasmic reticulum, though some comes form the ECF as well.
What type of pumps move calcium back into the SR of cardiac muscle?
SERCA pumps (need to relax the heart)
What type of transport is utilized by the SERCA pumps?
Primary transport
What are the mechanisms that pump calcium out of the cytoplams to cause cardiac muscle cell relaxation?
- SERCA pumps pumping calcium back into the SR (active transport)
- Sodium/Calcium exchangers on cell surface (secondary transport)
Explain why sodium/calcium exhangers on cell surface of myocytes are secondary transport?
They utilize the Na+ gradient created by Na+/K+ pumps (powered by ATP)
Troponin binds to which three things:
troponin A binds to actin
troponin T binds to tropomyosin
troponin C binds to Ca2+
In order for the myosin head (ATPase) to bind to actin filament for the crosbridge cycle, what needs to occur?
Ca2+ needs to bind to troponin c, which moves the tropomyosin-troponin complex out of the way, exposing the actin binding sites.
What do the numbers 0-4 mean on the diagram?
0- depolarizaton phase
1- slight repolarization
- platuea
- repolarization
- resting state
Which cardiac cells are not contractile?
Sinoatrial node cells
Why are action potentials longer in the cardiac tissue than with neurons?
It reduces the risk of tetany
Which 3 ions play the biggest role in cardiac action potentials?
Na+, Ca2+, K+
What is the relationships of K+, Na+, Ca2+, Cl-, and pH when it comes to extracellular vs. intracellular spaces?
Na+, Ca2+, and Cl- all have higher concentrations outside of the cell, while, K+ has higher concentrations inside the cell. pH is higher outside vs. inside the cell.
The membrane potential will always be closest to the Nernst potential of the most permeable/soluble ion.
Permeable ion
Which ion is most permeable at rest?
K+
Which ion is most permeable during depolarization (phase 0)?
Na+
What is causing the slight repolarization at phase 1?
The Na+ channels close, but K+ still slowly leaking
What is happening at phase 2 (the plateau) during the cardiac action potential?
L-type (slow channels) voltage gated Ca2+ channels are open, allowing Ca2+ into cell, and K+ channels are also open, allowing K+ out of cell. They tend to balance eachother out.
During phase 3 (repolarization), what is occuring?
The Ca+ channels are beginning to close and more K+ channels are opening up
What is responsible for the resting membrane potential in the cardiac myocyte?
The inward rectifying current (K+)
What phase deals with the outward rectifying current (K+)?
Phase 1
What are and what is the function of the delayed rectifier K+ channels?
voltage-gated K+ channels that can be rapidly or slowly activted upon depolarization.
What is the confirmation of the inactivation and activation gate of Na+ voltage gated channels in cardiomyocytes in phase 4 (resting potential)?
Activation gate is closed, and inactivation gate is open
What is the confirmation of the inactivation and activation gate of Na+ voltage gated channels in cardiomyocytes in phase 0 (depolarization)?
Inactivation and activation gate are both open
What is the confirmation of the inactivation and activation gate of Na+ voltage gated channels in cardiomyocytes in phase 1 (slight repolarization)?
Activation open and inactivation closed
What is the confirmation of the inactivation and activation gate of Na+ voltage gated channels in cardiomyocytes in during repolarization down to the resting state?
activaton gate will close and the inactivation gate will open
What do you call the time period in which the inactivation gate is closed and in which an action potential is not possible?
Refractory period
What is the difference between relative refractory periods and absolute refractory periods?
Absolute is that an action potential will not fire and relative refractory period is that an action potential is possible if there are enough open inactivation gates.
Study figure for possible hyperkalemic consequences
What happens to the resting potential with hyperkalemia?
The resting potential becomes less negative.
What is affected during hyperkalemia?
Increased conduction time, reduced resting potential, reduced action potential size and slowed rate of rise.
Weaker heart beat
During the action potential plateau, which ion is most important?
Ca2+ ions flowing through the L-type voltage gated channels and acivating the CICR on the sarcoplasmic reticulum.
What affect does adrenaline have on an action potential in the heart?
Adrenaline enhances the platuea calcium current.
What effect does tetrodotoxin (TTX) have on the action potential?
TTX blocks the fast Na+ channels, abolishing the initial spike depolarization.
What is the effect of sympathetic stimulation on action potentials in the heart?
Phase I plateau increases and heart rate increases.
How does foxglove (digitalis) affect the heart?
Foxglove (digitalis) increases the contractile force and intracellular Ca2+ concentration in muscle by blocking the Na+/K+ pump on the K+ side.
K+ blocked, Na+ stays inside cell, hence- no Na+ gradient driving force to push Ca2+ out of cell, so-Ca2+ stays inside, hence- stronger contraction
What is phospholamban (PLB) and what is it’s function?
They are connected to the SR calcium ATPases and act as the “breaks” and slows them down, pumping less Ca2+ back into cell
What affect does the sympathetic system have on phopholamban?
It allows the phospholamban breaks to ease up a bit and allow more Ca2+ into the SR which gets the cell ready for the next beat (relaxation, restitution, diastole)
Explain the process of the effect of noradrenaline on heart B1 -GPCR- AC receptors?
How does activated protein kinase A affect the L-type voltage gated Ca2+ channel and phospholamban (PLB) on the SR in the cardiomyocyte?
it induces a greater influx of Ca2+ into the cell and inhibits PLB “breaks” which in turn allows the Ca2+ Ase on the surface of SR to pump more Ca2+ into the SR to prepare for the next beat.
What is the function of verapamil in the heart?
It is a calcium channel blocker
