CVS - Cellular And Molecular Events Flashcards Preview

Semester 2 > CVS - Cellular And Molecular Events > Flashcards

Flashcards in CVS - Cellular And Molecular Events Deck (35):
1

Which pump DOES NOT set the resting membrane potential?

What is the role of this pump?

Na+/K+ ATPase (sodium pump)

To establish the gradients

2

What are the concentration of ions intracellularly and extracellularly?

K+

Na+

Ca2+

Cl-

3

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

How is the electrical gradient formed?

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

4

When does the net outflow of K+ ions stop?

When the equilibrium potential is reached.

At Ek, there is not net movement of ions

5

Why does the resting membrane potential not equal the equilbrium?

Ek -95mV RMP = -90mV

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

6

What is the role of cardiac myoctyes?

Fire action potentials

They are electrically active

7

What does an action potential in a cardiac myocyte cause?

Why is this required?

Triggers an increase in cytosolic Ca2+

Increased is required to allow actin and myosin interaction

8

Describe the ventricular (cardiac) action potential.

Be able to draw

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

9

Why is the Ca2+ influx important?

For triggering contraction

10

Describe the SA node action potential

What is the initial slope to threshold called?

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)

11

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

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

12

At what membrane potential is a pacemaker potential activated?

More negative than -50mV.

The more negative, the more it activates

13

What are HCN channels?

What do they allow?

Hyperpolarisation-activated Cyclic Nucleotide- gated channels

Allow influx of Na+ ions which depolarise the cells

Only in pacemaker potential

14

What does the pacemaker potential cause?

Slow depolarisation to threshold

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

15

Which is the fastest node to depolarise?

What does it do?

SA node

Sets the rhythm, is the pacemaker

16

What is the route of the SA node?

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

Describe cardiac muscle

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

18

What do gap junctions allow?

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

What do dermosomes do?

Rivet cardiac cells together structurally

20

What effect does depolarisation have on the Ca2+ channels?

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

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

Where are these channels located?

Opens the calcium induced calcium release channels in the sarcoplasmic recticulum

22

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

25% enters across sarcolemma

75% released from sarcoplasmic recticulum (intracellular stores)

23

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

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

Discuss excitation-contraction coupling in cardiac cells.

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

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

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

Skeletal = triad

Cardiac = diad

26

What happens when calcium binds to troponin C?

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

(Same as skeletal muscle)

Revise sliding filament theory

27

In relaxation what must happen to Ca2+?

How is this achieved?

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

How is the tone of blood vessels controlled?

Where are these cells located?

What cells are they present in?

By contraction and relaxation of vascular smooth muscle cells

Smooth muscle cells located in tunica media

Present in arteries, arterioles and veins

29

What is the structure of vascular smooth muscle?

Actin and myosin filaments not sitting in nice striated pattern

Actin and myosin filaments connected to dense bodies and radiate out

30

Discuss excitation and contraction coupling in smooth muscle cells?

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

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

What inhibits MLCP?

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

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

Must be phosphorylated

33

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

Inhibits action of myosin light chain kinase

Inhibits phosphorylation of the myosin light chain and inhibits contraction

34

What initiates contraction of vascular smooth muscle cells?

Depolarisation

or

Activation of alpha adrenoreceptors

35

How is the resting membrane potential set?

What channels are open at rest?

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