What is it about?
The electrical activity in the heart, which initiates contraction and blood pumping to circulation, depends on Na+ entry into the myocardial cells via proteins in the membrane that act as Na+ channels. This study shows that the Na+ channel proteins in the neonatal heart show differences from those present in the adult heart, and evidence indicates that these differences play an important role in the lower myocardial excitability (i.e., diminished sensitivity to triggers of electrical activity) also detected in the immature myocardium. This study also shows that, differently from adults, myocardial cells of neonatal rats accumulate Na+ in their cytoplasm during cyclic electrical/contractile activity, apparently due to increased activity of a protein that exchanges Na+ and Ca2+ across the membrane.
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Why is it important?
The lower excitability may protect the neonatal heart from arrhythmias, but may also require more intense stimuli for cardiac pacemaking and defibrillating. On the other hand, the greater Na+ accumulation in neonate cardiac cells may have impact on several cell functions, including contractile activity, metabolism and adaptation to changes in pH. This finding is surprising because Na+ accumulation, here observed in the myocardium of healthy neonates, has been reported in adults only in pathological conditions, such as heart failure and diabetes.
Read the Original
This page is a summary of: Developmental differences in myocardial transmembrane Na
transport: implications for excitability and Na
handling, The Journal of Physiology, May 2022, Wiley, DOI: 10.1113/jp282661.
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