Theme 3: Lecture 18 - The molecular and ionic basis of cardiovascular control Flashcards
What is the H band
The part with only thick filaments and no overlapping thin filaments
What is the A band
All the thick filaments, it will have some overlapping thin filaments
What is the I band
The area that has thin filaments only
What is the M line
Where the thick filament cell bodies are
What is the Z line
What holds 2 sarcomeres together
How does the Frank Starling law affect force of contraction of cardiac muscle
- Increased contractility
- Longer and stronger
- “More crossbridges means more of everything”
- Intrinsic regulation
How does sympathetic activity affect the force of contraction of cardiac muscle
- Faster and stronger
- NOT longer duration
- “Extant crossbridges work harder and faster”
- Extrinsic regulation
How does an increased end diastole volume lead to an increased force of comtraction
- When the sarcomeres are fully stretched there is an increased overlap of thick and thin filaments
- More overlap leads to more force generators
- Which leads to a stronger contraction
What is heart rate mostly determined by
The slope of the pacemaker potential
How does sympathetic stimulation lead to a faster heart rate
- Noradrenaline leads to an increased of If (Net inward current). This increases slope of pacemaker potential via Beta 1 receptor
- Noradrenaline leads to an increase in ICa which leads to an increased force of contraction
- Noradrenaline leads to an increase in IK. IK = delayed rectifier which shortens AP duration allowing a faster HR
Describe the funny current (If)
- Net current is inward
- Conducts both Na in and K out
- “non-specific monovalent cation channel”
- The reversal potential of If is -10 mV
- It is NOT a sodium channel
- HCN Channel opens when membrane gets more negative
- Controls slope of pacemaker potential
- Na/Ca exchange also helps with PP
How does parasympathetic stimulation lead to a slower heart rate
- Acetylcholine leads to a increase in K current IK(Ach) which hyperpolarizes membrane
- decreases slope pacemaker potential
Describe an acetyl choline K channel
- G protein (Gi coupled)
- Muscarinic
How does atropine increase heart rate
It blocks vagal slowing of the heart rate
Name 3 different types of K channels in cardiomyocytes
- Delayed rectifiers
- Inward rectifiers
- ACh sensitive K channels
When are inward rectifier K channels open
When the voltage goes below -60mV and stay open until the next depolarisation
When are the delayed rectifier K channels open
In repolarisation and after hyperpolarisation
The refractory period
When there is so much positive current leaving the cell, it is impossible to depolarise it again
Why is the voltage in after hyperpolarisation more negative than at rest
-Both the delayed rectifiers & inward rectifiers are open during early AHP
-The inward rectifiers open when the membrane is more negative than -60 mV
The delayed rectifiers are still open during the AHP -b/c they are slow to close
-At rest the delayed rectifiers are closed
-During AHP: the ↑ K+ permeability and ↓ Na+ permeability means the membrane potential moves very close to EK
What is the effective refractory period
When it becomes nearly impossible to start a new action potential
How long does the effective refractory period last in cardiomyocytes
The whole duration of the AP
Why does the effective refractory period last for the the duration of the AP in cardiomyocytes
- Protects the heart from unwanted extra action potentials between SA node initiated heart beats
- Extra APs could start arrhythmias
Describe T tubules
- Membrane currents can be near contractile machinery
- Contiguous with extracellular fluid
- Adjacent to SR
- T tubule depolarises leads to
- Terminal Cisterna detects it leads to
- Terminal cisterna sends it throughout SR
What are T tubules
Invaginations of plasma membrane into myocyte
What are Terminal Cisternae
Enlarged area of the SR
Describe terminal cristernae
- Continuous with SR
- Specialised for storing and releasing calcium
