Exam 1 Review: Chapter 18: Physiology of Contraction
voltage-gated fast Na+ channels - An integral membrane protein ion channel for sodium ions found in the outer cell membrane of cardiac muscle cells which rapidly* opens and closes in response to a change in membrane potential (voltage); such channels are primarily responsible for the initiation of the action potential which triggers myocardial fiber contraction; sodium ions move into the cytoplasm when these channels open. [* rapidly in comparison to similar channels in skeletal muscle]
voltage-gated slow Ca++ channels - An integral membrane protein ion channel for calcium ions found in the outer cell membrane of cardiac muscle cells which opens and closes slowly in response to a change in membrane potential (voltage); such channels are primarily responsible for the persistence of depolarization (plateau) which prolongs the contraction and refractory period of cardiac muscle cells; calcium ions move into the cytoplasm when these channels open.
voltage-gated K+ channels - An integral membrane protein ion channel for potassium ions found in the outer cell membrane of cardiac muscle cells which opens in response to a change in membrane potential (voltage); such channels are primarily responsible for terminating an action potential and ending the contraction and refractory period of cardiac muscle cells while initiating repolarization; potassium ions move out of the cytoplasm when these channels open.
rapid depolarization - The change in membrane voltage potential which quickly triggers the action potential and contraction of cardiac muscle cells; the change is due to the opening of voltage-gated fast Na+ channels which allow Na+ ions to enter the cytoplasm causing the resting potential of -90 mV to change to +25 mV in the cell interior.
unstable resting potential - The membrane potential of a cardiac muscle cell, when it is not depolarized and contracting, is less constant than a corresponding skeletal muscle cell, due to primarily to the increased permeability ("leakiness") of its cell membrane to Na+ and K+ ions; as a result, cardiac muscle cells depolarize more easily, even in the absence of an external stimulus; this gives rise to their property of autorhythmicity. [Differences in sodium, calcium and potassium concentrations inside and outside the cardiac muscle cell and the action of the Na+/K+ ATPase pump produce the resting potential with a typical value of -90mV.]
pacemaker potentials - The action potentials or depolarization events of the conducting cells within the sinoatrial (SA) node within the heart; these cells are characterized as having no true resting potential, but instead generate regular, spontaneous action potentials; unlike most other cells that elicit action potentials (e.g., neurons, skeletal muscle cells), the depolarizing current is carried primarily by relatively slow, inward Ca++ currents instead of by fast Na+ currents; (in fact, unlike most other cells, there are no fast Na+ currents operating in SA nodal cells).
plateau - The relatively stable period (approximately 200 msec) during which cardiac muscle cells are depolarized and contracting as a result of the opening of he voltage-gated slow Ca++ channels; it is essentially the same time period as the refractory period.
repolarization - the restoration of a polarized (resting) state in the outer cell membrane of a cardiac muscle fiber following contraction; the change is due to the closing of gated fast Na+ and slow Ca++ channels and the opening of gated K+ channels which allow K+ ions to exit the cell cytoplasm causing the resting potential of -90 mV to be restored from the +25 mV in the cell interior during depolarization.
refractory period - The time interval, after a muscle fiber has been stimulated and a contraction has been achieved, which has to pass before the muscle cell can be stimulated to contract again; it is prolonged in cardiac muscle.
5. the sequence of events in the action potential in a contractile fiber of the heart. (Include the events in the ion channels involved.)
(1a) norepinephrine from the Sympathetic Division of the ANS stimulates a given conducting myofiber or contractile cardiac muscle cell to depolarize; or,
(1b) an adjacent conducting myofiber or contractile cardiac muscle cell transfers its depolarization through gap junctions in the intercalated disc to stimulate a neighboring conducting myofiber or contractile cardiac muscle cell to depolarize.
(2) the external stimulus triggers opening of either (1a) chemically-gated or (1b) voltage-gated sodium (Na+) channels which permits a rapid influx of sodium (Na+) ions which will lead to the events which trigger contraction.
(3a) the initial depolarization of the outer cell membrane is transmitted along the length of the cell and throughout the cell interior via a T-tubule system.
(3b) meanwhile the sodium (Na+) channels are closing and the sodium-potassium ATPase pumps are continuing to operate.
(4a) this wave of depolarization triggers the opening of slow calcium (Ca++) (voltage-gated ) channels in the outer cell membrane which permits a slower and more prolonged influx of calcium (Ca++) ions into the general cytoplasm.
(4b) this wave of depolarization triggers the opening of ordinary voltage-gated calcium (Ca++) channels in the smooth endoplasmic reticulum which permits an additional influx of calcium (Ca++) ions into the general cytoplasm.
(5) the arrival of the additional calcium (Ca++) ions into the general cytoplasm triggers the sliding filament mechanism of contraction of the cardiac cell's myofibrils.
(6) while the slow calcium (Ca++) channels remain open, the cardiac cell remains depolarized and in contraction.
(7) eventually the slow calcium (Ca++) channels begin closing while the voltage-gated potassium (K+) channels open, and the cardiac cell begins to repolarize; this will end contraction.
(8) soon afterward, the potassium (K+) channels close and the continuing operation of the sodium-potassium ATPase pumps restores the resting state and resting potential.
Sketch and Label:
8. a myogram and a graph of the action potential of a typical cardiac muscle contraction, including the ion channels and ion flows involved.
|The figure on the left depicts the myogram with the blue curve which tracks the electrochemical events of depolarization and repolarization (membrane potential on the Y axis to the left). In the same figure, the green curve depicts the force of contraction during the same time period (tension on the Y axis to the right). The figure on the right is not a myogram. However, it does illustrate the individual ion flows which are responsible for the shape and duration of the depolarization and repolarization of the cardiac muscle cell. To answer this question on an exam, you would want to indicate on your drawing of the figure on the left, that the rapid rise in the blue myogram to a peak is due to sodium ion (Na+) influx through fast gated sodium channels, the plateau is due to the prolonged calcium ion (Ca++) influx through slow calcium channels, and the repolarization (the rapid fall from 0 to - 80 mV) after the plateau is due to the removal of calcium ions (Ca++) from the cytoplasm by active transport at the same time that potassium ions (K+) are leaving the cytoplams due to the opening of the voltage-gated potassium (K+) channels. See the figure at the bottom as a possible model.|
6. the specific hormones and ions which regulate the heart rate and indicate what their specific influences on HR are.
|Hormone or Ion||Regulation of Heart Rate|
|epinephrine = adrenalin and norepinephrine||increase heart rate and have a positive inotropic effect (increase contractility independent of rate)|
|thyroid hormones T3 & T4||increase heart rate|
|calcium (Ca++) ions||hypercalcemia will increase heart rate; hypocalcemia will decrease heart rate|
|sodium (Na+) ions||hypernatremia will decrease heart rate; hyponatremia will increase heart rate|
|potassium (K+) ions||hyperkalemia will decrease heart rate; hypokalemia will increase heart rate|
11. the advantages to cardiac muscle cells because they have a long absolute refractory period (compared to skeletal muscle cells).
The main advantages of the long absolute refractory period in cardiac muscle cells are (1) prevention of tetany (sustained contraction) which would inhibit pump efficiency and (2) opportunity for a relatively long single twitch contraction to empty the chambers followed by a relatively long period of relaxation which permits the chambers to be refilled again.