Cardiac muscle Flashcards
what is cardiac muscle composed of
cardiac myocytes (myocardial muscle cells) which are shorter, branched cells and usually contain a single nucleus.
what connects cardiac myocytes?
intercalated disks– composed of desmosomes and gap junctions
how do the t tubules in cardiac muscle compared to sk muscle?
fewer T tubs, but larger and wider t tubs
Smaller amounts of sarcoplasmic reCculum -cardiac muscle requires the entry of extracellular Ca2+
An abundance of mitochondria (~1/3 of cell volume) -oxidaCve metabolism for ATP producCon
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how is contraction initiated in myocytes?
not by neurons; generated by autorhythmic cells; depol starts at SA node; APs generated spontaneously
describe the AP pattern in autoryth cells
funny current channels open at -60 mV, net influx of Na; around -45 mV, some t-type Ca channels open and If channels close; at -40 mV, L-type Ca channels open; Ca induced Ca released– lots of L type channels open allowing for a sharp depol to +15 mV; Ca channels close, K opens–> efflux of K to -60 mV; then If channels open again, etc
why is the SA node the dominant pacemaker?
has lots of HCN channels so reaches threshold faster that the rest of network—>region with most HCN channels set HR
describe an AP in a myocardial cell
Ions that entered from an AP are transferred to adjacent cells through gap juncCons leading to depolarizaCon of the cell.
- Once the adjacent cell reaches threshold voltage gated Na+ open causing the Na+ spike of acCon potenCal (green). (This AP also spreads to myocardial cells next to it through gap juncCons).
- The posiCve voltage change of the AP slowly opens L-type Ca2+ channels. -There is a brief repolarizaCon from fast K+ channels (blue) before the Ca2+ influx through the L-type Ca2+ channels cause the K+ channels to close and lead to a sustained depolarizaCon (the plateau) (yellow)
- once the Ca2+ channels close, slow K+ channels then open and hyperpolarize the cell (pink).
Excitation-contraction coupling in cardiac muscles
L-type Ca channels (DHP receptors) are not mechanically linked to RyR; depol flows through the membrane and causes Ca to enter through the L-type channels and bind to RyR on the SR to release more Ca–>sparks sum together–> this allows Ca to bind to sarcomeres; Ca-induced Ca released
relaxation in cardiac muscle
Ca unbinds from troponin; some Ca is pumped out into the ECF (moreso than in sk muscle) MOST of the Ca is taken back up into the SR
what regulates the SERCA pump?
PLN–PLN is active and activates the pump when phos;
how quicker relaxation(=quicker subsequent contraction) achieved?
reuptaking Ca faster
how is contractile force enhanced in cardiac muscle?
NOT through summation; in increase in ICF Ca in myocytes enhances contractile force;increased Ca2; length tension relationship
cardiac muscle is capable of graded single twitch contractions.
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how is contractile force enhanced in cardiac muscle through increased ICF Ca?
additional troponin complexes activated and
increased cross bridge formation leading to increased force of contraction
how is contractile force enhanced in cardiac muscle through length tension rlnshp?
cardiac muscle generates a higher force when slightly stretched
what does the sympathetic NS affect in the heart?
increases HR/conduction velocity
affects autorhyth. cells and contractile cells
how does the parasymp NS affect the heart?
decrease HR/conduction velocity– affects on autorhyth cells
how does the symp NS modulate contraction?
- Phosphoryla5on of Ca2+ channels causes the calcium channels to remain open longer during ac5on poten5als.
- Phosphoryla5on of ryanodine receptors enhances sensi5vity to Ca2+, increasing release of Ca2+ from the sarcoplasmic re5culum.
- Phosphoryla5on of SERCA (PLN) increases the speed of Ca2+ re-uptake which increases Ca2+ storage
explain the length tension rlnshp
- A slightly stretched sarcomere increases the Ca2+ sensi5vity of the
myofilaments.
-a stretched sarcomere has a decreased diameter which may reduce the distance that Ca2+ needs to diffuse increasing probability of cross-bridge cycling. - A slightly stretched sarcomere puts addi5onal tension on stress- ac5vated Ca2+ channels, increasing Ca2+ entry from extracellular space and increasing Ca2+ induced Ca2+ release.
when stretched, has a reduced diameter—>smaller distance of diffusion for Ca; more troponin complexes activated etc
Parasympathe5c neurons containing ACh mainly innervate the SA and AV node influencing autorhythmic myocardial cells, decreasing the frequency of ac5on poten5als (decreasing heart rate).
ACh acts on muscarinic cholinergic receptors opening K+ channels and closing T-type Ca2+ channels and HCN channels.
-since the pacemaker ac5vity does not usually reside within the AV node, these mechanisms act at the AV node to decrease conduc5on velocity.
Sympathe5c modula5on of pacemaker ac5vity
Beta1 adrenergic receptors can be ac5vated by NE released from sympathe5c neurons or epinephrine from the adrenal medulla
- increase Na+ conductance through HCN channels: cells reach threshold more rapidly
- increase Ca2+ conductance through Ca2+ channels:
- cells reach threshold more rapidly, shorter dura5on AP
what type of control is HR under?
tonic control
what is tonic control?
never really rests? stays at RMP for long?
