ion channels and transporters in the heart Flashcards
the heart is primarily made of myocyte cells and these can be divided into pacemaker and non-pacemaker cells. What are the non-myocyte cells in the heart
endothelial cells ( line the chambers) fibroblasts ( create extracellular matrix)
what do transporters do
allow passage of ions from one side of the cell membrane to the other but against their electrochemical gradient. Consequently energy is required in from of ATP
funny channels are voltage gated and mediated by cAMP , what ion is released from these channels
sodium into the cell - opens when membrane potential is negative
what drug inhibits a funny channel
ivabradine -slows HR when people are unable to take CCBs
affects phase 4
T type calcium channels are voltage gated opening at -50mV allowing calcium into the cell at phase 0 what channels do they prompt to open
T for transient so shut quickly
causes L type calcium channels to open
L type calcium channels allow calcium into the cell at phase 0 what at what voltage do they open
-40mV
what drugs block L type calcium channels
verapamil - calcium channel blocker
a delayed rectifier channel allows potassium OUT of the cell and is voltage gated but at what phase does this open
phase 3
allows repolariztion
more negative the more the gates close
blocked by class III antiarrhythmics
the anti porter NA/CA exchanger is voltage gated and is a form of secondary transport. How many sodium and calcium are exchanged
and what does this channel maintain
3 NA in for 1 CA out
maintains low conc of intracellular calcium
energy comes from sodium going down electrochemical gradient
the primary active transport NA/K atpase allows 2 K in for 3 NA out what does this maintain
intracellular sodium and potassium conc against their electrochemical gradients
what inhibits NA/K ATPase pump
digoxin
Digoxin induces an increase in intracellular sodium that will drive an influx of calcium in the heart and cause an increase in contractility. Cardiac output increases with a subsequent decrease in ventricular filling pressures
Digoxin exhibits its therapeutic and toxic effects by poisoning the sodium-potassium ATPase. The subsequent increase in intracellular sodium leads to increased intracellular calcium by decreasing calcium expulsion through the sodium-calcium, cation exchanger.
what cells are unable to generate their own AP
non-pacemaker cells
in non pace maker cells what is the major depolarising cation
sodium
in pacemaker cells what is the major depolarising cation
calcium
in non pace maker cells there are fast sodium channels they are voltage gated and allows sodium into the cell at phase 0 causing rapid depolarisation of the MP and becoming briefly positive , what blocks this
tetrodoxin from puffer fish
flecanide which is a Class 1 anti-arrhythmic drug - which slows depolarisation and so velocity of conduction through the heart