CVS Session 4- Cellular And Molecular Events In The Heart Flashcards Preview

SOPHIE'S ESA 2 > CVS Session 4- Cellular And Molecular Events In The Heart > Flashcards

Flashcards in CVS Session 4- Cellular And Molecular Events In The Heart Deck (14):
1

Why is the RMP not = to E potassium?

Because the membrane has a small permeability to other ions.

2

What are the membrane potential limits for a ventricular cardiac AP graph?

-95mV to +30mV

3

Describe a ventricular cardiac AP.

-spread of activity from pacemaker cells causes initial depolarisation to threshold.
-voltage gated sodium channels then open, allowing the movement of sodium into the cell and therefore depolarising the membrane.
-there is a slight repolarisation to approx 0mV due to a transient outward movement of potassium ions, NCX reversal and inactivation of sodium channels.
-there is hen a plateau phase caused by calcium channel opening.
-repolarisation is caused by the inactivation of calcium channels and opening of potassium ones, causing potassium to move out.

4

What are the limits of membrane potential for a SA node AP?

-60mV to +20mV

5

Describe an SA node AP.

-to begin, there is a slow, gradual depolarisation called the funny current which is due to sodium ions moving in through HCN (slow) channels that are activated when the membrane is negative.
-once the threshold is reached, this causes calcium channels to open and calcium to move in, causing depolarisation.
-the downstroke is caused by potassium channels opening and potassium ions moving out.

6

Why isn't the depolarisation in an SA node AP due to sodium ions?

Because the prolonged pacemaker potential caused by the funny current means that sodium channels become inactivated.

7

What is excitation- contraction coupling?

Cardiac myocytes are electrically active and therefore fire APs. This causes an increase in cytosolic calcium ions because the calcium ions that enter during the AP stimulates further CICR.
This calcium allows the coupling of actin and myosin because the calcium binds to calmodulin, which activates MLCK, which in turn Phosphorylates the myosin light chain and allows actin to bind.

8

What two structures: electrically couple and mechanically couple cardiac myocytes?

Electrically- gap junctions
Mechanically- desmosomes

9

How does relaxation of cardiac myocytes occur? (3)

Calcium is expelled from the cell via calcium ATPase or NCX, and is stored intracellularly in the SR using SERCA.

10

What is the tone of blood vessels controlled by?

Contraction and relaxation of vascular smooth muscle cells.

11

What are the two ways that contraction of VSM cells occurs?

-depolarisation
-activation of alpha adrenoreceptors

12

How does calcium entry through GPCRs cause contraction of VSM cells?

Calcium activates GPCRs, causing the G alpha q subunit to be released and turn PIP2 into IP3 and DAG.
IP3 binds to IP3 receptors on sarcoplasmic reticulum and cause calcium release from the SR.
This calcium binds to calmodulin (binds 4) which activates MLCK.
MLCK Phosphorylates the light chain of myosin, allowing actin to bind.
Contraction.

13

How does relaxation of VSM cells occur?

-MLCP dephosphorylates the light chain on myosin.

14

What contributes to the RMP?

-set by the permeability of the membrane to potassium ions as potassium channels are open, causing them to move out.
-this establishes a more negative potential inside than out= electrical gradient.

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