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39 Cards in this Set

  • Front
  • Back
What cells activate cardiac muscle cells to sponatneously depolarize?
Pacemaker cells
What feature connects cardiac muscle fibers
Gap junctions

conduct ions
Once one cardiac cell is excited, the impulse can sprad to allother cells.

"all-or-none"
Functional syncytium

Cannot adjust force by temporal/spatial summation
Excitation contraction coupling in skeletal...
Independent of extracellular calcium ions
What role does extracellular calcium ions play in cardiac cells?
Extracellular calcium ions are cruical for contraction
Where is the nuclei in cardiac muscle?

Skeletal muscle?
Cardiac: centrally located

Skeletal: subssarcolemmal (under PM)
How many nuclei per cell does cardiac muscle have?

Skeletal
Cardiac: one nucleus/cell

Skeletal: multiple nuclei/cell
List order of cardiac fibers in order of increasing size
Atrial<ventricular<purkinje fibers
List order of cardiac fibers in order of increasing length.
Atrial<ventricular<purkinje
Compare the striations of the cardiac fiber types
Atrial & ventricular: prominent

Purkinje: faint bc lack of contractile protein
Do cardiac cells have glycogen?

Which fibers have the most?

How does glycogen stain in H&E?
Yes

Purkinje have most

Stains lighter around nucleus
What makes-up the largest volume of organelles?
Myofibrils 50%
Mitochondira 33%
Where are the T-tubules located in cardiac m?

in skeletal m?
Along the Z line

Intersection of I and A bands
DiadsA
Formed by the SR cisternae & T-tubules
Atrial granules contain?

How is hormone released?
Secretory granules that contain
ANP.

Stretch releases ANP
-"spot welds"
-where PM of two cells come very close together
Macula aderenes (desmosomes)
-Where actin cytoskeleton comes out and joins intercalated disc

-Allows pulling on PM at a given region to transmit forces to next cell
Fascia adherens
How is the cardiac excitation-contraction coupling different from skeletal?
1. Ca crosses T-tubules through VOLTAGE-gated Ca channels (DHPR)

In skeletal, AP down T-tubule causes conformational change in DHRP which causes conformational change in ryanodine receptors...MECHANICAL change.


2. Activator Ca causes release of Ca from the SR via Ca releases channels (aka ryanodine receptors

In skeletal, Ca doesn't bind the receptor since it's a mechanical change.
How is Ca pump different in cardiac?
Calcium pumped out of the cells by Ca pump & Na/Ca exchanger.

Cardiac cells are MORE sensitive to Ca than skeletal muscle
the ability to develop contractile force at a specific muscle length
contractility
Length-Tension relationship
-Passive properties of cardiac cause stiffness near plateau that limits inc. in length. So it gets hard to stretch more.
Cardiac m operates on what two regions of the length-tension curve?
Operates on the ascending & plateau region

No one ever sees descending curve
Ascending region of the length-tension relationship
Stretch-->inc. Calcium-->more crossbridging
Descending region of the length-tension relationship
Due to decreased overlap of the myosin heads & actin sites.
When contractility is increased by elevating cAMP what happens?
1. Inc. contraction force
2. Inc. velocity of shortening at a load
3. Inc. speed of BOTH contraction & relaxation
How does NE inc. contractility?
NE-->B-adrenergic receptor-->Gs-->adenylate cyclase-->inc. protein kinase A
What proteins does Protein Kinase A phosphorylate?
1. Dihydropiridine receptor
2. Phospholamban
Dihydropiridine Receptor
Phosphorylated-->inc. in activator Ca-->binds to ryanodine receptor-->release of Ca from SR-->inc. cytosolic Ca-->inc. contractile force
Phospholamban
Protein associated with the Ca pump in the membrane of the SR
What happens when Phospholamban is phosphorylated?
Inc. pumping of Ca into SR
What are 2 benefits of Phospholaman?
1. Way to store more Ca
2. Sweeps Ca out of sytosol and into SR more quickly after excitation-->quick relaxation
Do nerves initatiate contraction in cardiac m?
No, but do adjust both heart rate & contractility
What is the role of sympathetic & parasympathetic nerves for cardiac m?
Sympathetic-->release NE-->inc. contracility

Parasympathetic-->release Ach-->dec. contractility
Why does force of contractility inc. when the heart rate inc (frequency of contraction)?
When freq inc., some Ca that should go into SR is left behind.

Temporary Ca build-up-->more actin-myosin interactions
Digitalis
ability to inhibit the Na/K pump

results in:
1. Inc. in intracellular [Na]
2. Slows down the Na/Ca exchanger
3. Inc. cytosolic Ca-->inc. crossbridges
How does digitalis slow down the Na/Ca exchanger?
-Na/Ca exchanger imports 3 Na in and 2 Ca out.
-If administer digitalis-->build-up of intracellular Na
-Less Na pumped in, less Ca pumped out
-MORE cytosolic Ca!
Decrease in contractility are caused by?
1. Dec. in cytosolic [Ca]
2. Dec. supply of ATP
+ inotropic agents caused?

- inotropic agents...?
Increase contractility

Decrease contractility
What are the effects of long term overstimulation of NE?
excess NE-->stimulation of MAP Kinase pathway-->cell division-->hypertrophy & apoptosis-->dec. in amount of cells-->heart failure