L10 Myocardial E-C Coupling Flashcards
Functional role of T Tubule
transmits electrical activity to the cell’s interior; located at Z lines
Functional role of Sarcolemma
propagates the AP down into the T tubule; Contains L-type Ca channels so controls Ca influx
Functional role of SR
Site of Ca storage
Terminal Cisternae is where CICR occurs to initiate contraction
Longitudinal Cisternae is where SERCA functions to take Ca back into the cell for relaxation
Functional role of Troponin C
Binds Ca when it’s available and moves the Tropomyosin/Troponin into the actin groove so actin/myosin can affiliate for contraction
Troponin/Myosin in Heart
is the same as in skeletal muscle. Same contraction mechanisms
Cellular mechanisms in E-C Coupling
- Impulse from pacemaker cell conducts down cell and is carried into the cell by T Tubules
- Depolarization causes slow inward Ca current via L-type Ca channels
- Ca in the cell can now bind and open RyR channels
- Ca released from SR and binds to Troponin-C
- actin-myosin motion
- SERCA takes Ca back into SR
- Ca also removed via Na/Ca exchange and random Sarcolemma pump
Cardiac vs. Skeletal: size
Cardiac: small
Skeletal: large
Cardiac vs. Skeletal: innervation
Cardiac: all innervated in syncytium – coupled via gap connections
skeletal: all cells innervated separately
Cardiac vs. Skeletal: electrical activation
Cardiac: cell-cell conduction
skeletal: NMJ using Ach
Cardiac vs. Skeletal: contraction with Ca
Cardiac: uses CICR with Ryr
Skeletal: voltage dependent DHPR activates RyR
doesn’t require Ca, requires voltage to be depolarized
Cardiac vs. Skeletal: contraction amplitude
Cardiac: larger amplitude = regulated by Ca influx in L-type and Ca content in SR
Skeletal: larger amplitude = frequency of APs summated and recruitment of more fibers
Cardiac vs. Skeletal: metabolims
Cardiac: aerobic; requires O2 -> 35% mitochondria
Skeletal: anaerobic -> 2% mitochondria
never infarcts
Factors that change contraction via changing Contractility: Catecholamines
NE, ie. - decreases time of relaxation & increases strength of contraction
positive inotropic effect - (definition of positive inotropic agent = something that increases CONTRACTILITY)
bind to B1 receptors, which make cAMP from ATP
cAMP activates PKA, which P’s *Ca channels (increases contraction strength by increasing influx), *phospholamban (enhances relaxation by enhancing SERCA activity), *Troponin-I, (enhances relaxation by inhibiting the binding of Ca to Troponin-C)
Factors that change contraction via changing Contractility: Cardiac glycosides
ie: digitalis - increases strength of contraction ONLY
positive inotropic effects
block Na/K pump, which conserves ATP
increases Na concentration inside therefore lowering gradient for Na to come in.
Decreases Na/Ca exchange, so Ca builds up inside
SR Ca content goes up, increasing contraction strength
BUT – overloading SR with Ca can result in DADs
Factors that change contraction via changing Contractility: Ca channel blockers
(Verapamil, Diltiazam, nifedipine) - increases Refractory period of slow response cells
negative inotropic effects on heart
Block Ca channels
Less Ca influx in heart
Less SR Ca content = decrease in contraction strength
good for treating arrhythmias bc is blocks slow Ca channel responses of AV node