THE CONTRACTION AND RELAXATION OF CARDIAC FIBERS

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Introduction

Contraction is always controlled by the central nervous system (CNS), which is comprised of the brain as well as the spinal cord. The brain always controls voluntary muscle contractions, while, on the other hand, the spinal cord controls involuntary reflexes. Cardiac fibers usually undergo a series of the coordinated contraction through calcium-induced calcium release, which is conducted through intercalated discs.

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According to previous research, that calcium and not potassium is the main determinant of myocardial contractility became evident when Ebashi and Kodama described troponin, as well as regulatory proteins in the thin filament, were discovered to be crucial for micromolar calcium concentrations to be able to activate the contractile proteins of skeletal muscle in vitro. Thus, in Cardiac muscles, contraction occurs via a phenomenon referred to as excitation-contraction coupling (ECC). The phenomenon illustrates the entire conversion process of an electrical stimulus into a mechanical response from neurons. An inward flux of the existing extracellular calcium ions in cardiac muscle through calcium channels on the T-tubules usually sustains the depolarization of cardiac muscle cells for longer duration. Thus, contraction in cardiac muscle happens through the model of contraction known as sliding filament. In this case, there is sliding of myosin filaments along actin filaments in order to lengthen or shorten the muscle fiber for contraction and relaxation.

Various changes in relaxation and contractility can be viewed as functional responses developing rapidly in general, over a duration of a few seconds or minutes. The responses are affected by mechanisms such as altered calcium fluxes as well as post-translational phosphorylations. In the process of the plateau phase of the action potential, calcium ions usually flow down a steep concentration gradient and gradually enters the myocyte. Most of this calcium then enters through the L-type channels, strategically located primarily at sarcolemmal/sarcoplasmic reticulum junctions.

Another example of research done previously shows that the transcriptional regulation modifies myocardial contractility, and was done 1962. In this case, ATPase activity was discovered to be depressed in myofibrils that were isolated from failing hearts. The influx of calcium then triggers the release of more calcium from the sarcoplasmic reticulum via ryanodine receptors. The calcium-triggered calcium release is in contrast to skeletal muscle, whereby the action potential directly triggers the release of calcium. Intracellular calcium, which at this juncture is free, interacts with the C subunit of troponin. Consequently, it leads to a configuration change in the troponin complex, allowing the interaction of actin with myosin. Cross bridge cycling takes place, resulting to the shortening of the sarcomere and the resultant muscular contraction. As the intracellular calcium concentrations are exhausted during repolarization, calcium then dissociates from troponin with the decrease of intracellular calcium concentration, resulting in relaxation.

Conclusion

The strength of a cardiac contraction may be varied through increasing the amount of free intracellular calcium. This can be done by altering the sensitivity of the myofilaments to calcium, or both. The latter takes place while stretching of the myofilaments. Myofilament calcium sensitivity reduces due to acidosis. High concentrations of magnesium and phosphate also impair cardiac function. In the meanwhile, catecholamines activates beta-adrenergic receptors found in the heart to produce a G-protein mediated increase in cAMP and the enhanced activity of protein kinase which is cAMP-dependent. This results to the phosphorylation of calcium membrane channels, facilitating calcium entry into the cell. Phosphorylation of myosin also occurs in this juncture and increases the rate of cross bridge cycling. Catecholamines increase the rate of calcium re-uptake into the sarcoplasmic reticulum, thus aiding relaxation.

Bibliography

Alpert, Nelson. In Myofibrillar Adenosine Triphosphatase Activity in Congestive Heart

Failure, 940–946. Am J Physiol, 1962.Ebashi, Sesturo, and Arthur Kodama. In A New Protein Factor Promoting Aggregation of

Tropomyosin, 107–108. Tokyo: J Biochem, 1965.