Action Potentials Flashcards
SA node
generates a spontaneous action potential
What are the major ion channels involved in the generation of spontaneous action potentials in the SA node?
- funny channel / HCN channel: sodium channels
- T-type calcium channels
- L-type calcium channels
- K+ channels
Which channel initiates an action potential in the SA node which ion is involved and where does it go? (during an action potential in the SA node)
If Funny current / HCN - influx of Na+ into the cell
Which calcium channel opens first? What is a general characteristic of the channel? (during an action potential in the SA node)
T-type calcium channel; slower and less influx of calcium than L-type
Which calcium channel opens second? What is a general characteristic of the channel? (during an action potential in the SA node)
L-type calcium channel; faster, greater influx of calcium and open for longer than T-type calcium channel
Which channel opens last during an action potential in the SA node? Which ion is involved and where does it go?
K+ channel allows K+ to flow out of the cell to achieve repolarization (return to resting membrane potential)
What are the three purposes of the AV node/bundle? What characteristics of their structure give them these abilities?
- Action potential entry limited to ventricles
- action potential delay to ensure enough ventricular filling
- backup pacemaker function should the SA node fail
- non-conducting fibrous sheath guard the atria and ventricles making the AV node/bundle the only pathway for action potential spread to the ventricles
- HCN channels present in the AV node (in less numbers than SA node) to produce spontaneous action potentials if the SA node fails
- smaller gap junctions in AV node compared to fast conducting cells which prevents action potentials from spreading really quickly because they have to travel through a smaller space
What are the major channels in ventricular myocyte action potentials?
- voltage-gated sodium channels
- L-type calcium channels
- Slow and Fast potassium channels
note that ventricular myocytes do not have HCN channels as they do not create spontaneous action potentials, they receive input from the purkinje fibers
What is the impact of B-adrenergic receptor activation on heart/SA node activity? What activates these receptors?
- Activated by epinephrine/norepinephrine released by sympathetic nervous system
- stimulate the SA node and increase heart activity
What is the impact of cholinergic receptor activation on heart/SA node activity? What activates these receptors?
- activated by acetylcholine released by the peripheral nervous system
- inhibits SA node/heart activity
What is the role of PKA, adenylyl cyclase and cAMP in cholinergic/B-adrenergic receptor activation?
- adenylyl cyclase is activated or inhibited by receptor binding (depending whether B-adrenergic or cholinergic)
- when ACTIVATED, adenylyl cyclase turns ATP into cAMP
- cAMP can activate PKA which can increase calcium release by phosphorylating and opening L-type Ca2+ channels
These functions are all inhibited in cholinergic receptor activation, as well as K+ channel targeting slowing the generation of action potentials
How is the heart affected by pregnancy?
heart becomes hypertrophic - myocytes grow larger to meet greater needs of host + fetal bodies. This induces a greater heart rate, stroke volume and thus a greater overall cardiac output
What is the general mechanism thought to be the reason behind cardiac changes during pregnancy?
- NOT b/c of sympathetic nervous system (epi/norepi) - INTRINSIC heart mechanism!
- increase in HCN2 channels in SA node
- increases action potential generation
What can happen in a pathological sense when there is an increased number of HCN2 channels in the heart
- increases chance of arryhthmias
- more action potentials paired with less potassium results in a delay in repolarization and allows for action potential generation prior to the end of the previous one
What is the role of GRK2?
- phosphorylates B-adrenergic receptors and tags them for degradation to decrease receptor activation under conditions of stress
- Decreases cAMP and PKA by replacing the stimulatory portion of the G protein with an inhibitory one
- Tries to prevent overworking of heart, but under heart failure conditions it is overexpressed resulting in the heart’s inability to respond and maintain cardiac output
How do B-blockers work?
- block some B-adrenergic receptors
- prevents GRK2 upregulation and activation
- prevents desensitization to B-adrenergic receptors
What did Bct do in mice?
blocked the binding of GRK2 to the beta adrenergic receptor G protein
