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Lecture
Human Physiology
Friday, January 15, 2010
“CV VI”
Excitation-Contraction Coupling
•Ca required for contraction, but Ca can be highly toxic in high amounts; Ca compartments inside the
cardiac cell (sarcoplasmic reticulum [SR]) ensure that a source of Ca is close to the muscle
•Ca transport mechanisms
Sarcolemma
Ca channels (dihydropyridine [DHP] receptor) brings Ca IN; this is how Ca enters during
the “plateau phase”
Na/Ca exchanger moves Ca OUT (also capable of bringing Ca in) using the concentration
gradient of Na (3 Na in exchange for 1 Ca)
Ca pump (ATPase) moves Ca OUT; relatively small/accessory role
SR (storage)
Ca pump (ATPase) moves Ca into SR; 1 mole of ATP moves 2 moles of Ca
•Phospholambin is an inhibitor of the pump; regulates Ca pump
Ca channel (ryanodine receptor) lets Ca OUT; Ca is able to induce Ca release through
this channel
•Sequence
AP arrives, which opens DHPR
Ca rushes in, and binds to ryanodine receptor
Ca released, and binds to troponin C in myofibrils, causing contraction
Ca dissociates, and most gets pumped back into SR, and some is pumped into the ECF by the
other transporters
•Ventricular muscle temporal relationships
Ventricular muscle cells remain depolarized for a long period of time
To have sustained heart rhythm. . . need electromechanical restitution
Once it depolarizes, it must repolarize (electrical restitution)
Once muscle contracts, it must relax again (mechanical restitution)
Cannot produce tetanic contractions in cardiac muscle as you can in skeletal muscle
Control of Heart Rate
•ANS can control heart rate
Sympathetic increase heart rate (positive chronotropic effect) and contractile force (positive
inotropic effect)
Mechanisms
•Produces nerves feeding the heart, which release norepinephrine, which later
binds to beta-adrenergic receptor (acts through adenylate cyclase to produce
increased concentrations of cAMP; increases Na & Ca permeability
oIncreased Na perm., increase rate of diastolic depolarization in SA node
(increase HR)
oIncreased Ca perm., increase force of contraction (more Ca activates more
myofilaments)
Parasympathetic decrease heart rate & force of contraction (negative chronotropic & inotropic
effects)
Results in ventricular escape (don’t receive stimulation from SA or AV node); in this
case, the Purkinje system develops a rhythm (40-45 bpm)
Mechanisms
•Parasympathetic nerves (i.e. vagus) release ACh, which interacts with its
muscarinic receptor; produces many effects
oIncrease K efflux (hyperpolarization)
oIncrease cGMP
oDecrease cAMP (antagonizes the sympathetic effect; anti-adrenal effects)
oTurnover of inositol phosphates
Note on Electrocardiogram
•Some of the electricity during the cardiac cycle is picked up at the surface of the skin, which provides
basis of ECG
•PR interval period of atrial depolarization through to the AV node (about 0.18s)
Shortens as heart rate increases
•QRS duration ventricular depolarization (about 0.08s)
•QT interval ventricular depolarization + repolarization (about 0.40s)
•ST interval (QT – QRS) ventricular repolarization (about 0.32s)
•U wave
Sometimes seen in ECG
Caused by repolarization of papillary muscle (the muscle the helps hold the AV valves in
position)
Connected to wall of ventricle on one side and to AV valves at other side