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Bpk 305 > Excitation-Contraction Coupling > Flashcards

Excitation-Contraction Coupling Flashcards

1
Q

How is contraction strength regulated in myocytes

A

Individual myocytes change contraction strength

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2
Q

What factors can regulate cardiac contraction

A
  1. Length dependent
    - frank starling relationship (F/SV vs EDV)
    - length tension relationship
  2. Length independent
    - changes in contractility that are not related to sarcomere length
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3
Q

How does the frank-starling graph change when increased contractility? what possible inotropes can cause this?

A

SV vs EDV: Shift left and up (causes smaller EDV)
Positive inotropes: noradrenaline, adrenaline, cocaine, amphetamines, digitalis (digoxin)

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4
Q

How does the frank-starling graph change when decreased contractility? what possible inotropes can cause this?

A

SV vs EDV: shift right and down (less blood pushed out, larger EDV)
Negative inotropes: propranolol, nifedipine, ACh

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5
Q

What are inotropes?

A

Inotropes are drugs that tell your heart muscles to beat or contract with more power or less power

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6
Q

How does sympathetic and parasympathetic stimulation effect contractility? State shifts of Frank-starling curve.

A

Sympathetic- increases contractility. Shift up and left.
Parasympathetic- decreases contractility. Shift down and right.

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7
Q

Define inotropy

A

Force of contraction

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8
Q

Define chronotropy

A

Rate of heart beating

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9
Q

Dromotropy

A

Rhythmicity ofcontraction

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10
Q

Where does excitation-contraction coupling begin

A

T tubules

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11
Q

What ways can myocytes use to vary contraction

A
  1. Change length of AP
  2. Amount of Ca2+ let into the cell from Cav1.2 channel OR sarcoplasmic reticulum (SR)
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12
Q

What is the name of the calcium channel in sarcolemma

A

Cav1.2

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13
Q

What releases Ca from the SR

A

Ryanodine receptor RyR2

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14
Q

How is calcium released from SR

A

Calcium enters cell through Cav1.2 channels in sarcolemma. This calcium binds to ryanodine receptors of SR and allows RyR2 to open releasing calcium. Mechanism- Ca induced, Ca release (CICR)

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15
Q

Name the L-type Ca channel, when does it open

A

Cav1.2
Opens at -35mV
Alpha1c subunit

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16
Q

Name the two calcium sources used in excitation-contraction coupling and state their contribution percents

A

Cav1.2- 10-40%
RyR2- 60-90%

17
Q

Is Ca moving up or down its concentration gradient when going through: Cav1.2 or NCX channels

A

Cav1.2- down gradient (into cell)
NCX- up gradient (out of cell)

18
Q

What does NCX channel exchange? How can it function like this?

A

3 Na into cell, 1 Ca out of cell (net +1 in)
Energy generated by Na in, is used to get Ca out

19
Q

How does SERCA-2A work? What does it pump?

A

2 Ca enter SR with the help of ATP (active transport)

20
Q

What is the role of PLB?

A

PLB- phospholamban inhibits ATP activity
For excitation- contraction coupling- it inhibits ATP used in SERCA-2A therefore no Ca re-absorbed into SR

21
Q

Name all the channels in the sarcolemma

A

Cav1.2
NCX
Sodium-potassium pump (3 Na out, 2 K in)

22
Q

How is cAMP used in myocytes vs sinoatrial node?

A

Myocytes: cAMP binds to protein kinase A (PKA) which phosphorylates phospholamban (PLB), Cav1.2, TnI

SAN: cAMP activates HCN channels

23
Q

What phosphorylates PLB and how does this effect PLB

A

PLB- phospholamban
PKA phosphorylates PLB
Causes PLB to detach from SERCA-2A- allowing more Ca reuptake

24
Q

What happens to force of contraction if SERCA activity is increased? How?

A

PKA increases SERCA activity
Force of contraction is increased
- faster relaxation
- more SR Ca release (b/c more uptake with PLB removed- so more load in SR)
- larger depolarization phase

25
Q

What three components of excitation-contraction coupling are increased by PKA activity? How do these components affect the force of contraction?

A

SERCA-2A activity
CA2+ entry via Cav1.2 channels
Relaxation rate
all increase force of contraction

26
Q

How does PKA affect Cav1.2 channels? What does this mean for the cell in general?

A

Phosphorylates channel, increases open probability.
This increases Ca current into cell and calcium-induced calcium release (CICR)
In general- increases force of contraction

27
Q

What is the outcome of PKA phosphorylating TnI

A

TnI directly bound to actin and TnC.
Phosphorylation causes a decreased affinity of TnC site II for Ca2+ (site II-initiate contraction). This promotes faster relaxation rate.
Overall force of contraction increases- Ca stripped faster therefore can be reused faster

28
Q

What is the sympathetic regulation pathway related to excitation-contraction coupling in myocytes

A

Noradrenaline binds to beta1 adrenergic receptor- Gs subunit leaves to activate adenylyl cyclase- creates cAMP- activates PKA- which then phosphorylates many things (PLB, Cav1.2, TnI, RyR)
RyR- increase fractional Ca release from SR

29
Q

Parasympathetic stimulation effect on excitation-contraction coupling

A

Decrease contractility, inhibit cAMP production therefore PKA can not be activated

30
Q

Pharmacological regulation of excitation-contraction coupling in full

A

Sympathomimetics - stimulate sympathetic NS
• cocaine - blocks NA re-uptake by neurons
• amphetamines - release NA from storage vesicles
• positive inotrope

Sympatholytics - inhibit the sympathetic NS
• β blockers (e.g. propranolol)
• negative inotrope

Digitalis (Digoxin)
• a positive inotrope
• inhibits Na/K-ATPase

31
Q

Pharmacological regulation of E-C coupling: what things stimulate sympathetic nervous system, provide examples

A

Sympathomimetics
Ex. Cocaine, amphetamines, positive inotropes

32
Q

Pharmacological regulation of E-C coupling: what things inhibit sympathetic nervous system, provide examples

A

Sympatholytics
Ex. Beta blockers (propranolol), negative inotropes

33
Q

What does cocaine do

A

Blocks noradrenaline re-uptake by neurons

34
Q

What do amphetamines do

A

Release noradrenaline from storage vesicles

35
Q

What does digitalis (digoxin) do and what problems does this cause E-C coupling

A

Inhibits Na/K ATPase (3Na out, 2K in). When no pump, the NCX channel works in the opposite direction Na out of cell and down gradient (b/c now high concentration inside). Ca into cell and down gradient.
normal NCX- 3Na into cell and down gradient, 2Ca out of cell and up gradient
Overall this will increase the resting membrane potential!

36
Q

Which pharmacological regulation increase the resting membrane potential? how?

A

Digitalis (digoxin)
Inhibit Na/K ATPase.
High Na concentration inside cell and reduction in K in cell increases resting membrane potential

Bpk 305 (10 decks)

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