Sessoion 4.2 Flashcards
How is the resting membrane potential set up?
1) Cardiac myocytes are permeable to K+ ions at rest
2) K+ ions move out of the cell down their conc gradient
3) small movement of ions makes the inside negative with respect to the outside as positively charged potassium ions leave the cell
4) as charge builds up an electrical gradient is established that is equal but opposite to the concentration gradient
What is the relationship between resting membrane potential and Ek?
Resting membrane potential does not exactly = Ek
- net outflow of k+ until Ek reached
- but resting membrane potential doesn’t equal Ek.
- very small permeability to other ion species at rest
How does excitation lead to contraction?
- cardiac myocytes are electrically active
- action potential triggers increase in cytosolic Ca2+
- a rise in calcium is required to allow actin and myosin interactions
What are the phases of a cardiac action potential?
1) rmp due to background k+ channels
2) upstroke due to opening of Na+ channels entering cell
3) initial repolarisation due to outward flow of k+
4) plateau in membrane potential as ca2+ channels open = influx of ca2+ balanced with efflux of k+
5) repolarisation as ca2+ channels close and k+ channels stay open
Why is the resting potential in the SAN weird?
The most negative it gets to is approx -60 mV after an action potential, then it starts slowly depolarising towards threshold
This is due to ion channels getting activated the more negative the cell gets, so once it reaches -60 the pacemaker potential/funny current can start
Why aren’t Na channels used in the SAN and whats used instead?
As the cell never gets that negative voltage gated Na channels would remain inactive all the time and so would be useless
Instead use voltage gated ca channels for upstroke depolarisation and k for downstroke repolarisation
What is the role of HCN channels in SAN action potential?
Allow influx of Na ions which depolarise the cell and aid the funny current
Which part of the heart depolarises to threshold the quickest?
The SAN
How can action potential firing affect HR?
Fire too slowly = bradycardia
Fails = asystole (no heart beat)
Too quickly = tachycardia
Random = fibrillation (if ventricles go into fibrillation, no co ordinated contraction of the heart)
Why are cardiac myocytes so sensitive to changes in k+?
K permeability dominates the resting membrane potential
What are the effects, risks and treatment of hyperkalaemia?
Effects
- Ek becomes less negative so the membrane doesn’t depolarise as much
- this inactivates some of the voltage gated Na channels = slow upstroke
Risks
- asystole
Treatment
- calcium gluconate (calcium acts as a charge shield against k)
- insulin and glucose (drives potassium ions into cells)
What does hypokalaemia do and what are the risks?
- lengthens the action potential
- delays repolarisation
The risks
- longer action potential can lead to early after depolarisation
- this can lead to oscillations in membrane potentials
- this can result in ventricular fibrilation
How does excitation lead to contraction?
- depolarisation opens L type ca2+ channels in t tubule system
- localised ca2+ entry opens calcium induced calcium release channels in SR
- close link between L type channels and ca2+ released channels
- 25% enters across sarcolemma, 75% released from SR
- ca binds to troponin c
- conformational change shifts tropomyosin to reveal myosin binding site on filament
How are cardiac myocytes relaxed?
Ca is pumped back into SR
- raised ca2+ stimulates the pumps
- across cell membrane, leave through sarcolemmal ca2+ ATPase or Na/Ca exchanger
How is the tone of blood vessels controlled?
Smooth muscle in the tunica media
