CVS Session 4- Cellular And Molecular Events In The Heart

Question 1

Why is the RMP not = to E potassium?

Answer 1

Because the membrane has a small permeability to other ions.

Question 2

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

Answer 2

-95mV to +30mV

Question 3

Describe a ventricular cardiac AP.

Answer 3

• 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.

Question 4

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

Answer 4

-60mV to +20mV

Question 5

Describe an SA node AP.

Answer 5

• 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.

Question 6

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

Answer 6

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

Question 7

What is excitation- contraction coupling?

Answer 7

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.

Question 8

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

Answer 8

Electrically- gap junctions

Mechanically- desmosomes

Question 9

How does relaxation of cardiac myocytes occur? (3)

Answer 9

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

Question 10

What is the tone of blood vessels controlled by?

Answer 10

Contraction and relaxation of vascular smooth muscle cells.

Question 11

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

Answer 11

• depolarisation

- activation of alpha adrenoreceptors

Question 12

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

Answer 12

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.

Question 13

How does relaxation of VSM cells occur?

Answer 13

-MLCP dephosphorylates the light chain on myosin.

Question 14

What contributes to the RMP?

Answer 14

• 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.