Cardiac Muscle

Cardiac Muscle Chapter

Cardiac myocytes

Cardiac myocytes

shorter branches cells that contain a single nucleus

intercalated disks

ends of cells where they link with other cells

desmosomes

link cells together mechanically at the intercalated disks

gap junctions

link cells together electrically at the intercalated disks

differences between cardiac muscles and skeletal muscles

less abundant but larger T tubules

smaller amounts of sarcoplasmic reticulum

larger amount of mitochondria

autorhythmic cells

specialized non contracting cells that generate action potentials spontaneously.

smaller and contain few contractile fibres

pacemaker potential

slow depolarization caused by hyperpolarization of I f receptors

what occurs at -40mV in autorhythmic cells

Ca2+ channels open, I f channels close

causes a quick spike of depolarization

what happens at +20mV in autorhythmic cells?

Ca channels close and K+ channels open causing repolarization of the membrane to -60mv

step 1 contractile AP

Sodium channels open causing a quick spike of depolarization in the cell

Step 2 of AP in contractile cells

peak depolarization is reached, causing Na channels to close

step 3 contractile AP

Ca channels open and fast K+ channels close, causing a plateau in potential

step 4 contractile potential

Ca channels close, Slow K channels open causing repolarization of the membrane back to resting potential of -90mV

How do autorhythmic cells and contractile cells connect?

gap junctions allow Ca from the autorhythmic action potential enter the contractile cell initiating an action potential

DHP receptors in cardiac muscle

DHP receptors are not mechanically coupled to ryanodine receptors therefore Ca2+ entry is necessary for contraction

calcium induced calcium release

calcium binds to RyR receptors and allows Ca release from the sarcoplasm

phospholamban

a protein that is a crucial regulator of cardiac contractility

when phospholamban is phosphorylated

Ca2+ pump inhibition is removed, enhancing relaxation rates and contractility

when dephosphorylated phospholamban

phospholamban inhibits the SERCA calcium pump

Increase in Ca effect

additional troponin complexes activated and increased cross bridge formation leading to increased force of contraction

Calcium concentration low effect

some actin remains covered by tropomyosin

Length tension relationship

cardiac muscle generates a greater force when slightly stretched

Sympathetic NS effect

increases heart rate/conduction and contractility (autorhythmic and contractile)

parasympathetic NS effect

decreases heart rate/conduction (autorhythmic only)

sympathetic modulation of contraction step 1

phosphorylation of Ca2+ channels increases calcium conductance during action potentials

sympathetic modulation of contraction step 2

phosphorylation of ryanodine receptors enhances sensitivity to Ca2+, increasing release of Ca2+ from the sarcoplasmic reticulum

sympathetic modulation of contraction step 3

increases rate of myosin ATPase

sympathetic modulation of contraction step 4

phosphorylation of SERCA increases the speed of Ca2+ reuptake which increases Ca2+ storage

theory 1 for cardiac length tension relationship

a slightly stretched sarcomere has a decreased diameter which may reduce the distance that Ca2+ needs to diffuse increasing probability of cross bridge cycling

theory 2 cardiac length tension relationship

a slightly stretched sarcomere puts additional tension on stress activated Ca2+ channels, increasing Ca2+ entry from extracellular space increasing Ca2+ induced Ca2+ release

tonic control of heart rate

autorhythmic cells can be modulated by sympathetic and parasympathetic neurons and thereofre heart rate is under tonic control

parasympathetic modulation

neurons containing ACh mainly innervate the SA and AV node influencing autorhytmic myocardial cells, decreasing the frequency of action potentials

parasympathetic effect of K channels

hyperpolarizes the resting potential, takes longer to reach threshold therefore slowing down the action potentials

parasympathetic effect on HCN channels

blocks some HCN channels causing slower depolarization, therefore decreasing AP frequency

Parasympathetic effect on T type Ca2+ channels

blocks some Ca channels, slowing down depolarization and therefore decreasing AP frequency

sympathetic modulation

beta 1 adrenergic receptors can be activated by NE released from sympathetic neurons or epinephrine from the adrenal medulla

sympathetic effect on HCN and Ca+ channels

increased Na+ conductance causes cells to reach threshold more rapidly and a decreased level of repolarization