Sodium Potassium Pump on the Propagation of an Action Potential

Discussion
Sodium and potassium could be seen as the dynamic duo critical for normal functioning of several processes in the body. In addition to assessing the role the sodium-potassium pump plays in the propagation of an action potential, this text will also highlight both the pathophysiologic impact of hyperkalemia on the action potential as well as the resulting clinical manifestations.
The Role of the Sodium-Potassium Pump on the Propagation of an Action Potential
In essence, messages sent by axons, according to Kalat (2012), are referred to as action potentials. In the context of this discussion, therefore, action potential has got to do with the electrical potential changes as a consequence of impulse passage along a nerve cell’s membrane.
The generation of action potential is dependent upon active transport pumps as well as a number of positive transport channels. With regard to the sodium-potassium pump (which is essentially a carrier protein), it is important to note that it comes in handy in the regulation of the concentration of ion on the cell membrane’s both sides via the movement of potassium ions into the cell, and sodium ions out of the cell (Toole and Toole, 2004). As Kalat notes (2012), outside the membrane, there is often a higher concentration of sodium ions than inside. Similarly, there is a higher concentration of potassium ions inside the membrane, than outside the membrane (Kalat, 2012). Basically, “as an action potential occurs at one point of the axon, enough sodium enters to depolarize the next point to its threshold, producing an action potential at that point… behind each area of sodium entry, potassium ions exit, restoring the resting potential” (Kalat, 2012, p. 44).
The Pathophysiologic Impact of Hyperkalemia on the Action Potential and Resulting Clinical Manifestations
In the words of Mushiyakh, Dangaria, Qavi, Ali, Pannone and Tompkins (2012), “the basic pathophysiology of hyperkalemic states involves either extracellular potassium shifts or decreased renal excretion” (43). For purposes of this discussion, therefore, hyperkalemia will be taken to be the elevation of blood potassium levels. Towards this end, hyperkalemia could either be mild, moderate, or severe – with potassium levels across the three states varying from 5.1 mEq/L to 7.0mEq/L or in some instances, higher. The abnormal potassium distribution constitutes one of the common etiologies as far as hyperkalemia measurement is concerned (Mushiyakh et al., 2012). It is important to note that abnormal potassium distribution could be witnessed in various circumstances. These include tissue damage, aldosterone deficiency, metabolic acidosis, adrenergic antagonists, and insulin deficiency (Mushiyakh et al., 2012). It is important to note that when extracellular potassium is elevated, neuron depolarization occurs as a consequence of the elevated resting membrane potential. Further, when extracellular potassium is elevated, muscle depolarization does not necessarily take place. This is more so the case given that muscle depolarization in this case occasions the flow of potassium out of the cell as a result of closure of the sodium inactivation gate. In this case, therefore, the muscle cell is repolarized.
The relevance of potassium when it comes to the normal nerve, heart, as well as muscle functioning cannot be overstated - in addition to activity control of various muscles, it plays an active role in the body’s nervous system by enabling normal electrical signal transmission. In that regard, therefore, abnormal potassium distribution could interfere with skeletal muscles functioning, and cause abnormalities in the electrical rhythm of the heart. In essence, “clinical manifestations of mild to moderate hyperkalemia are usually non-specific and may include generalized weakness, fatigue, nausea, vomiting, intestinal colic, and diarrhea” (Mushiyakh et al., 2012, p. 44). Hyperkalemia could also be occasioned by a weak pulse or a slow heartbeat. As Mushiyakh et al. (2012) further point out, severe hyperkalemia could in some instances lead to other conditions that are potentially life-threatening. These include muscle paralysis and cardiac arrhythmias.
Conclusion
In the final analysis, it is important to note that the relevance of appropriate potassium and sodium levels is critical to the proper functioning of the various processes of the human body. This is more so the case with regard to normal muscle contraction as well as nerve signals transmission, which is facilitated by molecular pumps.













References
Kalat, J.W. (2012). Biological Psychology (11th ed.). Belmont, CA: Cengage Learning.
Mushiyakh, Y., Dangaria, H., Qavi, S., Ali, N., Pannone, J. & Tompkins, D. (2012). Treatment and Pathogenesis of Acute Hyperkalemia. J Community Hosp Intern Med Perspect, 1(4), 39-46.
Toole, G. & Toole, S. (2004). Essential A2 Biology for OCR. Cheltenham: Nelson Thornes.