The to adequately relax to allow for adequate

The human heart is a mechanical pump that contracts and relaxes in a cyclical fashion. Contraction of the heart muscles  is necessary to ensure satisfactory perfusion of distal tissues, which require nutrients and oxygen for their metabolic needs.  Likewise, the heart is required to adequately relax to allow for adequate filling that will guarantee the requisite cardiac output (CO). CO is a product of the stroke volume (SV) and the heart rate (HR). Therefore, adequate left ventricular filling in a properly relaxed heart increases the SV and consequently the forward flow. Cardiac contraction occur during the systolic phase of the cardiac cycle while the heart relaxes during the diastolic phase of the cardiac cycle. The heart’s contractile apparatus consist of striated smooth muscles that are collectively known as cardiac myocytes. Each myocyte is furnished with a plasma membrane also known as sarcolemma, a rich network of mitochondria (because of high energy required in form of ATP), myofibrils (characterized by sarcomeric units of actin and myosin filaments), a rich network of calcium storage tubules (sarcoplasmic reticulum SR) and an extensive tubular network (T-tubules; facilitates Ca2+ transport). The actin and myosin filaments are major actors in contraction and relaxation of myocardium. The actin filament is a composite structure composed of two interwoven polymers of actin, three types of troponin (T, C and I) and tropomyosin (obstructs the binding sites for myosin at rest). Cross bridging of actin and myosin filaments results in sarcomere shortening or contraction and relaxation results from the return of the actin and myosin to their pre-contractile states. These two processes; contraction and relaxation, are highly dependent on energy in form of ATP. The sarcolemma is rich in L-type Ca2+ channels, a voltage gated channel that allows influx of  Ca2+ into the myocyte cytoplasm following a depolarization of the sarcolemma. The sarcolemma also contains other channels or transporters that are integral to the maintenance of intracellular Ca2+ homeostasis. The Na+/Ca2+ exchanger and the sodium pump (Na+/K+ ATPase) are important regulators of intracellular Ca2+ concentration which makes the latter an important target of a class of drugs that modify myocardial contraction. These and the sarcoplasmic reticulum Ca2+ ATPase (SERCA) act to keep intracellular calcium levels very low (10,000 fold less than external Ca2+ conc).

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