CVS Session 4 (Lecture 4.1) Flashcards Preview

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Flashcards in CVS Session 4 (Lecture 4.1) Deck (16):
1

What do action potentials cause generally within cardiac myocytes?

Increase in cytosolic [Ca2+]

2

Describe the ventricular/cardiac action potential stages.

1) RMP around -85mV
2) Around 200ms in, opening of VGNCs causes the upstroke and membrane depolarisation to +20mV
3) VGNCs inactivated and transient efflux of K+ current causes slight repolarisation
4) Plateau period caused by opening of VGCCs
5) 500ms in, membrane repolarisation occurs with VGCC inactivated and VGKCs open slowly causing K+ efflux

3

What type of VGCCs are opened during the plateau period?

L-type

4

Describe the SAN action potential stages.

1) Cell rests at pacemaker potential which varies and is depolarised slowly to threshold by a funny current (If) with an influx of Na+ (VGNCs are inactive) by HCN channels
2) Activated by membrane potentials more negative than -50mV
3) Opening of VGCCs to +20mV causes depol
4) Opening of VGKCs causes membrane repol to pacemaker potential

5

What does HCN channels stand for and what do they do? Under what circumstances are they activated?

Hyperpolarisation-activated cyclic nucleotide-gated channels. Allow Na+ influx in SAN depol. Activated under membrane hyperpolarisation.

6

What is special about the SAN?

Intrinsic electrical activity

7

Why does the SAN set the rhythm of the heart?

Fastest to depolarise therefore is the pacemaker.

8

What do desmosomes do in cardiac myocytes?

Provide mechanical adhesion to neighboring myocytes to allow coordinated contraction

9

What do gap junctions do in cardiac myocytes?

Provide electrical coupling to allow ions to move freely between cells. This allows the wave of depolarisation to spread from cell to cell.

10

Describe the process of calcium release in cardiac myocytes during systole.

1) Depolarisation opens L-type Ca2+ channels in T-tubules
2) Localised Ca2+ entry opens calcium-induced calcium release (CICR) channels in the SR via the ryanodine receptor.
3) 25% enters across sarcolemma, 75% released from SR.

11

What does the intracellular calcium released cause and how?

Causes contraction by binding to TnC. This confers a conformational change shifting tropomyosin to expose myosin binding sites in the actin filament.

Contraction occurs using the sliding filament model.

12

How is the intracellular Ca2+ release during systole returned to normal levels?

1) Most is pumped back into SR via SERCA
2) Some exits cell via sarolemmal Ca2+ ATPase
and NCX.

13

By what structure are the tone of blood vessels controlled?

Vascular smooth muscle cells located within the tunica media. Present in arteries, arterioles and veins

14

Describe the excitation-contraction coupling in vascular smooth muscle cells.

1) Activation of GPCR (Gaq) by stimulation of alpha-adrenoceptors
2) Generates IP3 and DAG
3) IP3 binds to IP3R on SR
4) Releases Ca2+
5) 4 x Ca2+ binds to calmodulin which activates MLCK
6) MLCK phosphorylates myosin (via ATP hydrolysis)
7) Allows mysoin light chain to interact with actin

15

What removes the phosphate on the light chain of myosin?

Myosin light chain phoshatase

16

What does PKA do to MLCK?

Phosphorylates it and inhibits MLCK thus no contraction.