Organization of heart muscle
Intercalated Discs
Direction through heart of cardiac conduction
Myocardial action potential current overview
Calcium-induced calcium release
Relationship between depolarization, Ca+2, Tension in cardiac myocyte
Contractile stuructre of sarcomere
Thin Filament
Thick Filament
Interaction b/w thick and thin filaments
Cross bridge cycling
Relaxation of sarcolemma
Contractility
Contractility is the intrinsic strength of contraction independent of loading conditions
Examples of how contractility is potentiated:
- oAdrenergic Signalling
- oPhosphorylation of phospholamban
- oPhosphorylation of troponin I
- oDigoxin
- oHeart rate Effects on Contractility
- oAscending Staircase
- oRest Potentiation
- oPost-Extrasystolic Potentiation
Adrenergic signaling in cardiomyocytes
Phospholamban and lusitropy
Digoxin mechanism
HR Effects: Ascending Staircase AKA Bowditch effect AKA Treppe
Post-Extrasystolic Potentiation:
Premature ventricular contraction (PVC, extrasystole) à less time for [Ca2+] to be removed from cell during relaxation (PVC beat itself is not strong because heart is in relative refractory period) à increased [Ca2+] available during heart beat à increased contractility of the post-PVC beat (post-extrasystole)
Preload effect on sarcomere length/Tension
Preload is tension “stretch” on the heart prior to contraction.
Passive length-tension: difference explained by titin (rather stiff spring, therefore skeletal with no titin not a real springy)
Starling’s Law: Greater Fiber Length-> More Developed Tension
Frank-Starling Curve
- •Increased Calcium Sensitivity at Greater Length, perhaps through greater actin/myosin proximity à More Contraction
- •Stretch-activated Ca2+ channels à More contraction
- •Old idea, not correct: more total overlap
Afterload
Afterload is the load against which muscle must contract.
We approximate afterload clinically with blood pressure.