electrical and molecular mechanisms in the heart and vascuculture Flashcards
how does potassium set up RMP (resting membrane potential)
high [K+] inside cell. few k+ channels are open meaning k+ diffuses out down the conc gradient BUT this takes + charge with it leaving side more negative. k+ therefore diffuses back in down the electrical gradient. once these are balanced = EK
why is RMP not equal to Ek
RMP is also affected by the membranes permeability to other ions
how are cardiomyocytes activated
they are activated by calcium. allows myosin and actin to interact.
describe the cardiac ventricular AP
RMP= -85. Na+ voltage gated channels open causing depolarisation (+30). peaks and then transient outward potassium current as K+ channels open (Ito) . Ca2+ channels open and calcium diffuses in and curve platues. calcium channels are then inactivated and more potassium channels open causing repolarisation and curve falls. cardiac ventricle has much longer action potential than others e.g axon.
describe the SAN AP
funny current causes slow automatic depolarisation until threshold reached by influx of Na+. curve increases due to opening of calcium voltage gated channels causing depolarisation. curve then decreases and voltage gated potassium channels open causing repolarisation.
how is the funny current started
all membranes more negative than -50mv causes activation of HCN channels (hyper-polarisation activated, cyclic nucleotide gated channels) which allow the influx of Na+ and depolarisation of the cell.
what is the SAN
sets the rhythm of the heart and is the fastest mycocyte to depolarise which is why the heart repose pm it to set of the wave of excitation because for example the purkinje fibres are much slower
describe thee route of the wave of excitation
starts at SAN and then goes to AVN where a delay is put in place to ensure that the atria finish contracting. then travels bundle of his and down to septum of heart before traveling up the ventricle walls via the purkinje fibres
what happens if AP fires too slowly? too quickly? fails to fire? or the electrical activity becomes random
bradycardia, systole, tachycardia and fibrillation
what is hyperkalaemia
when potassium levels are higher than 5.5mmol/L. this causes the Ek to get less negative so the membrane depolarises fit and inactivates some voltage gated sodium channels and slows the upstroke of the AP
what is hypokalaemia
when potassium levels are lower than 3.5mmol/L. some channels don’t function properly lengthening the AP and delaying repolarisation. during this time early after depolarisation may occur which open calcium channels causing oscillations leading to ventricular fibrillation.
why are cardiac myocytes so sensitive to potassium concentrations and cause arhythmia when changed
potassium sets up the resting membrane potential and they also have many types of potassium channels which act in parculiar ways.
describe the contraction of muscles
- depolarisation opens L type calcium channels via t tubules
- influx in calcium causing CICR channels to open in the SR
- calcium binds troponin causing conformational change which removes tropomyosin exposing myosin to bind with actin
- sliding filament mechanism
how do muscles relax again after contraction
calcium levels must return to normal. most calcium is pumped back into the SER via a pump called SERCA. some exits cell via calcium ATPase or sodium calcium exchangers
how does contraction in the tunica media of smooth muscle vessels take place to alter blood flow
calcium binds calmodulin after it enters via a channel and is catalysed by eosin light chain kinase. this then means it is able to phosphorylate regulatory light chain so it can bind actin
adrenaline binds adrenal receptors activating IP3 which releases Ca2+ from SR for binding to calmodulin and then above happens
DAG activates PKC which inhibits MLCP to sustain contraction
