Action Potentials and the Cardiac Cycle - Assignment Example

Action Potentials and the Cardiac Cycle Question Describe an action potential, the components of an action potential and the ionic movements that underlie them. According to Rothenberg and Chapman (1989), the so-called action potential is a series of electrical charges developed in a muscle and nerve cells, which leads to contraction. Seeley, Stephens, and Tate (2007) further explicated that action potentials in cardiac muscles, just like the skeletal muscles and neurons, are characterized by depolarization followed by repolarization, only that cardiac muscles do have a period of slow repolarization, which, in turn, causes a prolongation of the action potential. Moreover, action potentials in cardiac muscles would take approximately 200 to 500 milliseconds to complete and conducted from cell to cell, slower compared to less than 2 milliseconds in the action potentials in skeletal muscles (Seeley, Stephens, and Tate, 2007: 333). The following figures depict the stages or phases of an action potential: resting potential, depolarization, repolarization, and returning to resting potential or the final repolarization phase. Resting Potential Fig. 1. MCB-HHMI Outreach (2005). ‘Resting Potential’. The resting potential is the stage when the cell is not conducting an impulse (Rothenberg and Chapman, 1989). At this resting stage, the concentration of sodium (Na+) ions is higher outside the cell than the inside. On the other hand, the potassium (K+) ions are evidently higher inside the cell, compared to the outside. In this manner, the sodium-potassium pump is constantly at work to ensure a more positive ionic environment outside the cell membrane, thus leaving the cell interior highly negative (MCB-HHMI Outreach, 2005). Depolarization Fig. 2. MCB-HHMI Outreach (2005). ‘Depolarization’. Depolarization marks the first step in sending a signal or action potential, wherein the negatively charged cell interior is disturbed by the entrance positive Na+ ions, as we can see in the above figure (MCB-HHMI Outreach, 2005). Further, it is in this stage that Na+ channels open to give way to the diffusion of Na+ into the cell, at the same time, the K+ channels would just begin to open but closes immediately to decrease the permeability of cell to K+ (Seeley, Stephens, and Tate, 2007: 333). We can notice in figure 2 that the potassium and sodium channels are like gates that open to give way to their respective ions. Accordingly, the opening and closing of these membrane channels are responsible in the production of action potentials, as a result of the changes in cellular membrane permeability (Seeley, Stephens, and Tate, 2007: 333). In addition, calcium (Ca++) channels slowly open to cause Ca++ ions to diffuse into the cell, which also mimic depolarization (Seeley, Stephens, and Tate, 2007: 333). Repolarization OR the Early Repolarization Phase During this phase, the Na+ channels close, at the same time, some K+ channels open, thereby causes early repolarization (Seeley, Stephens, and Tate, 2007: 333). Fig. 3. MCB-HHMI Outreach (2005). ‘Repolarization’. Returning to Resting Potential OR the Final Repolarization Phase During this stage, the sodium-potassium pump restores the original concentrations of Na+ and K+ (MCB-HHMI Outreach, 2005), as depicted in the figure below. Fig. 4. MCB-HHMI Outreach (2005). ‘Returning to Resting Potential’. Question 2: How does an action potential result in muscular contraction? Describe the ionic movement that underlies this process (i.e. excitation-contraction coupling). An action potential triggers muscles cells, or myocytes, to contract by way of the process called excitation-contraction coupling (ECC) Klabunde (2007). In regard to the ionic movement that underlies this process, Klabunde (2007) further explicated the following: 1. When a myocyte is depolarized by an action potential, calcium (Ca++) ions enter the cell during phase 2 of the action potential through L-type calcium channels located on the sarcolemma. 2. This calcium triggers a subsequent release of calcium that is stored in the sarcoplasmic reticulum (SR) through “ryanodine receptors”, which are calcium-release channels. 3. The calcium (Ca++) that is released by the SR eventually increases the intracellular calcium (Ca++) concentration from about 10-7 to 10-5 M. 4. The free Ca++ binds to troponin-C (TN-C) that is part of the regulatory complex attached to the thin filaments. 5. When calcium binds to the TN-C, it induces a conformational change in the regulatory complex. In this manner, the troponin-I (TN-I) exposes a site on the actin molecule that is able to bind to the myosin ATPase located on the myosin head. 6. This binding results in ATP hydrolysis that supplies energy for a conformational change to occur in the actin-myosin complex. 7. The result of these changes is the so-called “ratcheting”, which refers to a movement between the myosin heads and the actin. In this manner, the actin and myosin filaments slide past each other, thus, shortening the sarcomere length. 8. Ratcheting cycles occur as long as the cytosolic calcium remains elevated. At the end of phase 2, calcium entry into the cell slows and calcium is sequestered by the SR by an ATP-dependent calcium pump (SERCA, sarco-endoplasmic reticulum calcium-ATPase), thus lowering the cytosolic calcium concentration and removing calcium from the TN-C. At a smaller scale, the cytosolic calcium is transported out of the cell by the sodium-calcium-exchange pump. 9. The reduced intracellular calcium induces a conformational change in the troponin complex leading, once again, to TN-I inhibition of the actin binding site. 10. At the end of each cycle, a new ATP binds with myosin head, thereby displacing the ADP and restoring the initial sarcomere length. (Klabunde, 2007) ________________________________________________ Question 3: Explain the Mechanical Events of the Cardiac Cycle. The Cardiac Cycle Illustration Fig. 5. Klabunde (2008). ‘Cardiac Cycle - Atrial Contraction (Phase 1): A-V Valves Open; Semilunar Valves Closed’ Fig. 6. Klabunde (2008). ‘Cardiac Cycle - Isovolumetric Contraction (Phase 2): All Valves Closed’ Fig. 7. Klabunde (2008). ‘Cardiac Cycle - Rapid Ejection (Phase 3): Aortic and Pulmonic Valves Open; AV Valves Remain Closed’ Fig. 8. Klabunde (2008). ‘Cardiac Cycle - Reduced Ejection (Phase 4): Aortic and Pulmonic Valves Open; AV Valves Remain Closed’ Fig. 9. Klabunde, R. E. (2008) ‘Cardiac Cycle - Isovolumetric Relaxation (Phase 5): All Valves Closed’ Fig. 10. Klabunde (2008). ‘Cardiac Cycle - Rapid Filling (Phase 6): A-V Valves Open’ Fig. 7. Klabunde (2008). ‘Cardiac Cycle - Reduced Filling (Phase 7): A-V Valves Open’ Explanation Cardiac cycle is a term that denotes a repetitive pumping process, which starts with the onset of cardiac muscle contraction and ends with the beginning of the next contraction (Seeley, Stephens, and Tate, 2007). Furthermore, according to Klabunde (2008: ‘Cardiac Cycle’), there are two basic stages in a single cardiac cycle activity. These are the diastole, which the first stage, and systole, the second stage, respectively. The diastole represents ventricular filling and a brief period just prior to filling at which time the ventricles are relaxing, whereas, the systole represents the time of contraction and ejection of blood from the ventricles (Klabunde, 2008: ‘Cardiac Cycle’). Hence, Seeley, Stephens, and Tate (2007) detailed the following mechanical events that take place during a cardiac cycle: 1. Contraction of the ventricles causes pressure in the ventricle to increase. Almost immediately, the AV valves close (the first heart sound). The pressure in the ventricle continues to increase. 2. Continues ventricular contraction causes the pressure in the ventricle to exceed the pressure in the pulmonary trunk and aorta. As a result, the semilunar valves are forced open and blood is ejected into the pulmonary trunk and aorta. 3. At the beginning of ventricular diastole, the ventricles relax and the semilunar valves close (the second heart sound). 4. The AV valves open and blood flows into the ventricles fills to approximately 70% of their volume. 5. Thereby, the atria contract and complete ventricular filling. 6. And the cardiac cycle begins again. (Seeley, Stephens, and Tate, 2007: p. 338) ________________________________________________ Bibliography Klabunde, R. E. (2008) ‘Cardiac Cycle’ [Online]. Available at: http://www.cvphysiology.com/Heart%20Disease/HD002.htm (Accessed: 11 June 2009). Klabunde, R. E. (2008) ‘Cardiac Cycle - Atrial Contraction (Phase 1): A-V Valves Open; Semilunar Valves Closed’ [Online image]. Available at: http://www.cvphysiology.com/Heart%20Disease/HD002.htm (Accessed: 10 June 2009). Klabunde, R. E. (2008) ‘Cardiac Cycle - Isovolumetric Contraction (Phase 2): All Valves Closed’ [Online image]. Available at: http://www.cvphysiology.com/Heart%20Disease/HD002.htm (Accessed: 10 June 2009). Klabunde, R. E. (2008) ‘Cardiac Cycle - Rapid Ejection (Phase 3): Aortic and Pulmonic Valves Open; AV Valves Remain Closed’ [Online image]. Available at: http://www.cvphysiology.com/Heart%20Disease/HD002.htm (Accessed: 10 June 2009). Klabunde, R. E. (2008) ‘Cardiac Cycle - Reduced Ejection (Phase 4): Aortic and Pulmonic Valves Open; AV Valves Remain Closed’ [Online image]. Available at: http://www.cvphysiology.com/Heart%20Disease/HD002.htm (Accessed: 10 June 2009). Klabunde, R. E. (2008) ‘Cardiac Cycle - Isovolumetric Relaxation (Phase 5): All Valves Closed’ [Online image]. Available at: http://www.cvphysiology.com/Heart%20Disease/HD002.htm (Accessed: 10 June 2009). Klabunde, R. E. (2008) ‘Cardiac Cycle - Rapid Filling (Phase 6): A-V Valves Open’ [Online image]. Available at: http://www.cvphysiology.com/Heart%20Disease/HD002.htm (Accessed: 10 June 2009). Klabunde, R. E. (2008) ‘Cardiac Cycle - Reduced Filling (Phase 7): A-V Valves Open’ [Online image]. Available at: http://www.cvphysiology.com/Heart%20Disease/HD002.htm (Accessed: 10 June 2009). Klabunde, R. E. (2007) ‘Excitation-Contraction Coupling’ [Online]. Available at: http://www.cvphysiology.com/Cardiac%20Function/CF022.htm (Accessed: 11 June 2009). MCB-HHMI Outreach (2005) ‘Depolarization’ [Online image]. Available at http://outreach.mcb.harvard.edu/animations/actionpotential.swf (Accessed: 9 June 2009). MCB-HHMI Outreach (2005) ‘Repolarization’ [Online image]. Available at: http://outreach.mcb.harvard.edu/animations/actionpotential.swf (Accessed: 9 June 2009). MCB-HHMI Outreach (2005) ‘Resting Potential’ [Online image]. Available at: http://outreach.mcb.harvard.edu/animations/actionpotential.swf (Accessed: 9 June 2009). MCB-HHMI Outreach (2005) ‘Returning to Resting Potential’ [Online image]. Available at: http://outreach.mcb.harvard.edu/animations/actionpotential.swf (Accessed: 9 June 2009). President and Fellows of Harvard College and MCB-HHMI Outreach (2005) ‘MCB-HHMMI Outreach (Animation by Matthew Bohan)’. [Online] Available at http://outreach.mcb.harvard.edu/animations/actionpotential.swf (Accessed: 9 June 2009). Rothenberg, M. A., and Chapman, C. F. (1989) ‘Dictionary of Medical Terms for the Nonmedical Person’. 2nd edition. New York: Barron’s Educational Series, Inc. Seeley, R. R., Stephens T. D., and Tate, P. (2007) ‘Essentials of Anatomy & Physiology’. 6th edition. Boston: McGraw-Hill Higher Education. Read More