Cardiovascular Control 1 Flashcards
How is resting membrane potential established?
membrane more permeable to K ions so diffuse down [] gradient carrying positive charge with them
not permeable to negative charge so incident chamber becomes more positive
electrical gradient opposes concentration gradient and equilibrium reached when they equal
What is used to predict equilibrium potentials?
Example for K (Ek)
Nerst equation - depends on flow of ion out of cell
[K] outside = 5mM
[K] inside = 120mM
Ek = -80mV (near RMP of ventricular myocyte)
K[] maintained by Na/K ATPase that pumps K into cell against [] gradient
Ek = RT/ZF ln[K]o/[K]i
What is the resting membrane potential (diastole)?
K+ equilibrium potential (Ek)
because at rest (diastole) the membrane is only permeable to K
What is the equilibrium potential for Na? ENa
[Na]o = 140mM [Na]i = 10mM ENa = +66mV
When does membrane potential = ENa?
during upstroke of action potential
What is the Goldman-Hodgkin-Katz Equation?
membrane potential is better described when the relative permeability of all ions is considered simultaneously
E(mv) = 61log Px[x]i + y + z
—————————
Px[X]o + y + z
What can change membrane potential?
permeability of membrane to ions
What is RMP for a ventricular myocyte?
-90mV
RMP depends on flow of K out of the cell
IK1 flows during diastole to stabilise the RMP - membrane is more negative
Why does depolarisation not reach equilibrium potential of Na in nerve cell?
Na+ channels inactivate as potential becomes positive to stop the outflow of Na
K permeability increases so positive charge flows out of the cell to restore membrane potential
What is the absolute refractory period?
time where no action potential initiated regardless of stimulus intensity
What is relative refractory period?
period after ARP where action potential elicited if stimulus strength is larger than normal
What is the difference between nerve and cardiac AP?
nerve shorter (2-3ms) cardiac (200-300ms) duration of the action potential controls the duration of heart contraction so for the heart to be an effective pump it must have a long and slow contraction
What determines cardiac action potential at rest?
K+
membrane is largely permeable to K to stabilise membrane potential
What physiological mechanism reduces the risk of arrhythmia in cardiomyocytes?
a large stimulus is required to excite the cell
What happens during Phase 0?
= UPSTROKE
AP causes a large change in Na permeability of the cardiomyocyte
Influx of Na
What happens during Phase 1?
= EARLY REPOLARISATION
Large intracellular Na inactivates Na channels and reduces PNa - Na channels enter ARP
Increase in permeability to K
K leaves the cell causing notch in graph (TO/ transient outward potassium current starts)
What happens during Phase 2?
= PLATEAU
Large intracellular Na[] increases PCa early in plateau via LTCC
Influx of Ca triggers CICR release from Ca stored for contraction
Increase Ca intracellular and efflux of K maintains plateau at 0mV to allow prolonged AP
What happens during Phase 3?
= REPOLARISATION
PCa decreases and PK increases (slow and small)
LTCC inactivated slowly
Repolarisation by normal K channel causes IK1 K channels (other subtype) to open
What is the full recovery time?
time at which a normal AP is elicited with a normal stimulus
What is the significance of refractory periods?
Recovery time is caused by Na inactivation
Na channels reactivate as the membrane repolarises
RP is good for the heart to allow it to fill before next stimulus causes a contraction
What is the difference in RP between skeletal and cardiac muscle?
Skeletal - repolarisation occurs early in contraction phase so restimulation and summation of contraction is possible and a second AP can quickly be stimulated
Cardiac - long RP so you cannot re-excite the muscle until the contraction is already well underway
Muscle cannot be tetanised
What is tetanus?
sustained contraction following series of stimuli
Which K channel is responsible for fully repolarising the cell?
IK1
large current that stabilises the membrane potential to reduce the risk arrhythmia. Gradual activation of K currents (K outward of cell) balances and overcomes Ca influx
activated once the cell is partially repolarised
during RRP
How to reduce contraction of smooth muscle to prevent hypertension?
Ca influx blocked by dihydropyridine Ca channel antagonists that bind to LTCC and block it
NIFEDIPINE, NITRENDIPINE, NISOLDIPINE
