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Semester 2 > CVS - Cellular And Molecular Events > Flashcards

CVS - Cellular And Molecular Events Flashcards

1
Q

Which pump DOES NOT set the resting membrane potential?

What is the role of this pump?

A

Na+/K+ ATPase (sodium pump)

To establish the gradients

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2
Q

What are the concentration of ions intracellularly and extracellularly?

A

K+

Na+

Ca2+

Cl-

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3
Q

How does the K+ permeability set the resting membrane potential?

How is the electrical gradient formed?

A

K+ ions, more inside the cell than outside so they move down their concentration gradient

Small movement of K+ ions out of the cell leaves the inside of the cell -ve charged.

As charges builds up an electrical gradient is established

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4
Q

When does the net outflow of K+ ions stop?

A

When the equilibrium potential is reached.

At Ek, there is not net movement of ions

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5
Q

Why does the resting membrane potential not equal the equilbrium?

Ek -95mV RMP = -90mV

A

RMP is not as negative as Ek due to there being a small permeability to other ion species

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6
Q

What is the role of cardiac myoctyes?

A

Fire action potentials

They are electrically active

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7
Q

What does an action potential in a cardiac myocyte cause?

Why is this required?

A

Triggers an increase in cytosolic Ca2+

Increased is required to allow actin and myosin interaction

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8
Q

Describe the ventricular (cardiac) action potential.

Be able to draw

A

Upstroke due to opening of voltage gated Na+ channels (depolarise)

Initial repolarisation due to transient outward K+ channels

Plateau due to opening of voltage gated Ca2+ channels (repolarise). balanced with K+ efflux.

Repolarisation due to efflux of K+ through voltage gated K+ channels open. Ca2+ channels inactivated

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9
Q

Why is the Ca2+ influx important?

A

For triggering contraction

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10
Q

Describe the SA node action potential

What is the initial slope to threshold called?

A

Unstable membrane potential = Pacemaker potential- If (funny current) influx of Na+

Upstroke = Opening of voltage gated Ca2+ channels (depolarise)

Downstroke = Opening of voltage gated K+ channels (repolarise)

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11
Q

Why is the upstroke in a SA node action potential not with Na+ ions?

A

Na+ chanenls would have inactivated if they are slowly activated even by -60mV.

Very few Na+ channels in pacemaker cells

Note - initial pacemaker potential slow depolarise is with Na+ ions

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12
Q

At what membrane potential is a pacemaker potential activated?

A

More negative than -50mV.

The more negative, the more it activates

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13
Q

What are HCN channels?

What do they allow?

A

Hyperpolarisation-activated Cyclic Nucleotide- gated channels

Allow influx of Na+ ions which depolarise the cells

Only in pacemaker potential

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14
Q

What does the pacemaker potential cause?

A

Slow depolarisation to threshold

By which time the Na+ channels will have been inactivated that’s why there is an influx of Ca2+ ions

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15
Q

Which is the fastest node to depolarise?

What does it do?

A

SA node

Sets the rhythm, is the pacemaker

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16
Q

What is the route of the SA node?

A

Across right atrium
Down the septum
And up the bundle of his and up the sides of the ventricles - causing the ventricles to contract from the bottom

17
Q

Describe cardiac muscle

A 
Striated muscle
Branching pattern
Single central nucleus
Cells connected at intercalated discs
Gap junctions
18
Q

What do gap junctions allow?

A

Movement of ions and electrical coupling of cells

Effectively large ion channels - allow rapid transfer of electrical activity between one cell and the other

19
Q

What do dermosomes do?

A

Rivet cardiac cells together structurally

20
Q

What effect does depolarisation have on the Ca2+ channels?

A

Opens the L type Ca2+ channels in the T tubule system

The Na+ ions depolarise the cell, this depolarisation causes the Ca2+ channels to open

21
Q

What effect does the entry of Ca2+ have on the calcium induced calcium release channels?

Where are these channels located?

A

Opens the calcium induced calcium release channels in the sarcoplasmic recticulum

22
Q

What is the percentage of calcium that enters across sarcolemma and from sarcoplasmic recticulum?

A

25% enters across sarcolemma

75% released from sarcoplasmic recticulum (intracellular stores)

23
Q

What is the difference between the requirement for Ca2+ in skeletal muscle and cardiac muscle?

A

Skeletal muscle does not need an influx of Ca2+ as a conformational change can cause Ca2+ release

Cardiac muscle requires Ca2+ entry to contract

24
Q

Discuss excitation-contraction coupling in cardiac cells.

What pump is used to allow Ca2+ to go back into the SR?

A

Excitation = Ca2+ moves into the cell
This opens the calcium release channel on the SR
Ca2+ is released from SR
Ca2+ from extracellular calcium goes on to bind to troponin C to trigger contraction.

Relaxation - need to remove Ca2+ from the cell, 25% goes out through channels, 75% goes back to SR through SERCA pump

25
Q

What type of t tubules are in skeletal and cardiac muscle?

A

Skeletal = triad

Cardiac = diad

26
Q

What happens when calcium binds to troponin C?

A

Causes a conformational change, shifting tropomyosin to reveal myosin binding site on actin filament

(Same as skeletal muscle)

Revise sliding filament theory

27
Q

In relaxation what must happen to Ca2+?

How is this achieved?

A

Must return to resting levels

Most is pumped back into the SR via the SERCA pump
Raised Ca2+ stimulates the pumps

Some exits across the cell membrane via Na+/Ca2+ exchanger
Sarcolemma like Ca2+ATPase

28
Q

How is the tone of blood vessels controlled?

Where are these cells located?

What cells are they present in?

A

By contraction and relaxation of vascular smooth muscle cells

Smooth muscle cells located in tunica media

Present in arteries, arterioles and veins

29
Q

What is the structure of vascular smooth muscle?

A

Actin and myosin filaments not sitting in nice striated pattern

Actin and myosin filaments connected to dense bodies and radiate out

30
Q

Discuss excitation and contraction coupling in smooth muscle cells?

A

Depolarisation opens the voltage gated Ca2+ channels –> influx of Ca2+–> binds to calmodulin–> activates MLCK (myosin light chain kinase) which phosphorylates the myosin light chain to permit interaction with actin

Relaxation as Ca2+ levels decline –> MLCP dephosphorylates myosin light chain, makes myosin inactive

31
Q

What happens in terms of excitation contraction coupling when noradrenaline activates alpha 1 receptors?

What inhibits MLCP?

A

Causes production of Gq receptors –> stimulates IP3 –> causes release of calcium from SR–> calcium binds to calmodulin which activates MLCK to activate myosin

Protein kinase C

32
Q

What must happen to the myosin light chain to enable actin-myosin interaction?

A

Must be phosphorylated

33
Q

What does phosphorylation of Myosin light chain kinase (MLCK) by Protein kinase A do?

A

Inhibits action of myosin light chain kinase

Inhibits phosphorylation of the myosin light chain and inhibits contraction

34
Q

What initiates contraction of vascular smooth muscle cells?

A

Depolarisation

or

Activation of alpha adrenoreceptors

35
Q

How is the resting membrane potential set?

What channels are open at rest?

A

RMP is set largely due to K+ permeability of the cell membrane at rest

Leak K+ channels are open at rest

Na+/K+ ATPase pump DOES NOT set the RMP

Semester 2 (26 decks)

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