7. Cellular and Molecular Events in the CVS Flashcards
Talk through the opening and closing of relevant channels in a ventricular or cardiac action potential.
There is opening of voltage gated Na+ channels that cause the rapid depolarisation. There is a transient outward K+ current. Then voltage gated Ca2+ channels open to stop the repolarisation. Ca2+ channels inactivate and the voltage gated K+ channels open to return the membrane potential to resting.
What do the numbers: 0, 1, 2, 3, and 4, correspond to on ventricular and cardiac action potentials?
0 = depolarisation 1 = transient repolarisation 2 = plateau 3 = repolarisation 4 = resting potential.
Talk through the SA node action potential.
Pacemaker potential gives an initial slope to the threshold by the funny current of Na+ influx. When the threshold, -50mV, is met, voltage gated Ca2+ channels open and there is the upstroke. The downstroke is caused by opening of V-gated K+ channels.
What is the structure of cardiac muscle?
Signal central nucleus, cells joined at intercalated disks, gap junction permit movement of ions and electrically couple cells, desmosomes rivet cell together.
How does depolarisation cause increased cytosolic calcium?
It opens L-type Ca2+ channels in T-tubule system (25% of Ca2+ entry). Localised Ca2+ entry opens calcium induced calcium release channels in the SR (75% of Ca2+ entry).
How are cardiac myocytes relaxed after excitation?
Return of [Ca2+]i to normal, resting levels. Most Ca2+ is pumped back into SR via the SERCA (stimulated by raised Ca2+), some exits across the cell membrane - sarcolemmal Ca2+ATPase and Na+/Ca2+ exchanger.
Why does the myosin light chain need activating for cardiac muscle contraction?
So they can interact with actin. Only activated, phosphorylate myosin light chains can bind to actin for contraction.
How is contraction of vascular smooth muscle regulated?
Ca2+ binds to calmodulin and activated myosin light chain kinase, this phosphorylated the myosin light chain to permit interaction with actin. Ca2+ levels decline and there is relaxation as the myosin light chains dephosphorylate. If MLCK is phosphorylate by PKA, its own action is inhibited.
Talk through shape of ventricular and cardiac action potentials.
There is a rapid upstroke and depolarisation. There is then a transient repolarisation before an extended plateau. Finally there is repolarisation to the resting potential.