P: Cardiac muscle

Question 1

How does the AP spread from the SA node

Answer 1

The sinoatrial node is capable of its own spontaneous depolarisations, which causes APs
It spreads through coupled cells, gap junctions through the atria and via the atrio ventricular node to the ventricles

Question 2

Describe contraction + relaxation of cardiac muscle

Answer 2

Voltage-gated Ca channel (DHPR receptor) facilitates calcium entry from ECF –> induces calcium release from SR
During relaxation, SERCA takes up calcium in SR, but calcium must also be extruded to ECF via:
- Na/Ca transporter (3 Na+ in, 1 Ca2+ out)
- ATP (pumps out Ca)

Question 3

How is force of contraction in cardiac muscle increased

Answer 3

An increase in intracellular Ca2+
Increased stretch on CM as an intrinsic mechanism for increasing force of contraction

Question 4

What is isoproterenol

Answer 4

A β-agonist which increases the intracellular calcium transient which in turn increases the force of contraction

Question 5

Effect of SNS on heart

Answer 5

Release of adrenaline/noradrenaline
Binds to receptors on the cell membrane
Increase in cAMP levels –> increases PKA
Leads to phosphorylation of several proteins in the muscle cell e.g. voltage-gated Ca channel + SR phospholamban
This means more Ca2+ released from SR so more actin-myosin cross-bridges –> greater force of contraction
Ultimately during SNS stimulation, time for diastole and systole decreases

Question 6

Intrinsic mechanism to increase contraction

Answer 6

Increased stretch:
By effect of titin to increasing no. of actin/myosin interactions And by increased sensitivity to any available Ca2

Question 7

What is titin?

Answer 7

Because titin is attached to both myosin and actin, stretching of titin brings them closer together, increasing the chances of contact between both filaments. Anchors actin to Z discs