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Lecture 7

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University of Toronto St. George
Michelle French

Lecture 7  Cardiac Muscle: Excitation-Contraction coupling  The movement of Na, Ca and K ions lead to one of the most used clinical tests, ECG  1) The action potential spreads through the muscle fiber's network of T-tubules, depolarizing the inner portion of the muscle fiber  open Na+ channels close  2) Voltage (sensitive) gated L-Type Ca2+ channels open due to depolarization, Ca2+ enters the cell  Calcium concentration in the extracellular matrix is 2-5 millimolar  Calcium concentration, generally in most cells, is 1-2 micromolar  a thousand fold difference between extracellular and intracellular  3) Ca2+ flows along the gradient, inducing Ca2+ release via Ryanodine Receptor channels (RyR) on the sarcoplasmic reticulum  Calcium concentration in the SR is 0.5 millimolar  4) Local release causes Ca2+ spark  5) Ca2+ cascade causes Ca2+ signal  6) Ca2+ ions bind to Tropin C, Tropin T pulls the inhibitory troponin, Tropin I, away and opens a pocket for Myosin head to bind, leading to contraction  “This is happening every second”  7) Relaxation happens when Ca2+ unbinds from Tropin C  8) Ca2+ is pumped back into the sarcoplasmic reticulum for storage  9) 1 Ca2+ ion is exchanged for 3 Na+ by the NCX antiporter embedded in cell membrane  10) Na+ gradient is maintained by the Na+-K+ ATPase  3 Na+ ion is pumped out while 2 K+ moves in  Note:  There are about 5-6 main protein involved in the muscle contraction  Actin myofilaments - Tropomyosin (bound to Actin) binds troponin I, C, and T  Myosin - Myosin Rod, Head and Binding Protein C  Cardiac Action Potential  Two general types of action potential   1) Non-Pacemaker action potentials  “Fast response” action potential  Rapid depolarization  Throughout the heart, except for pacemaker cells  1) Pacemaker  generate action potential, “trigger”  Less than a 1000 cells in the entire heart that generate the spontaneous action potential  “Slow response” action potential  Slower rate of depolarization  Found in the Sinoatrial (SA node) and Atrioventricular (AV node) of the heart  In circumstances of failure in the SA and AV node, the purkinjie fibers can be acting pacemaker cells  Cardiac action potentials are unique  Both pacemaker and non-pacemaker action potentials in the heart differ considerably from action potentials found in the neural and skeletal muscle cells  Main difference is:  Nerves: 1 ms  Skeletal muscle cells: 2-5 ms  Stable at -70 mV  Net Na+ entry through Ach operated channels  Very rapid repolarization  Almost no refractory period, allowing for muscle twitch  Fas stimulation will result in continuous contraction as the refractory period is short - NOTE: A refractory period is the time following an action potential during which a normal stimulus cannot trigger a second action potential  Cardiac action potentials range from 200 to 400 ms.  Pacemaker Stable at -60mV, Non-Pacemaker Stable at -90mV  The refractory period lasts almost as long as the muscle twitch  If we stimulate at any time during the refractory period, nothing will happen  The big benefit between being able to stimulate at any time to generate new contractions (in skeletal muscles) versus the heart  If we could stimulate the heart during the refractory period, it would lead to heart arrhythmia;  Autorhythmic nature of cardiac cells  Less than a thousand (out of trillions) cells among the myocardial cells, the pacemakers, generate the action potential that is sent to neighboring cells via gap junctions  What is the underlying reason that the heart cells contract?  Unstable membrane potential  Unlike these -90mv stable myocardium membranes, the pacemakers aren’t as stable, -55mv to -60mv  This unstable membrane potential is called a pacemaker potential or non-resting potential. Whenever the pacemaker potential reaches threshold, the autorythmic cell firs an action potential is fired.  This pacemaker is due to an ion channel that generates what is called the funny current, I f  f channels are permeable to both K+ and Na+  When the cell membrane potential is -60mv, I chfnnels open  The I channels belong to a family of HCN channels, or f hyperpolarization-activated cyclic nucleotide-gated channels  When open, Na influx > K efflux  Roles of Na+ and Ca2+ ions in depolarization  Nerve and muscle cells  Depolarization caused by an opening of sodium channels  This also occurs in non-pacemaker cardiac cells  Cardiac Pacemaker cells  Ca2+ are involved with initial depolarization phase of action potential  In the pacemaker, it is largely the calcium ions that are responsible rather than Na+ ion  Cardiac non-pacemaker cells  Ca2+ influx prolongs the duration of the action potential and produces a characteristic plateau phase  Effect of pacemaker activity  This mV potential is then transmitted to adjacent cells (gap junction)  Propagating action potentials causing contraction  Electrical conduction in myocardial cells  Depolarization of autorythmic c
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