Review on Sodium Calcium Exchanger (Na+-Ca2+X) Electrophysiological Characteristics and its Role in Cardiac Arrhythmias

Abstract

Cardiac arrhythmias is one of the cardiovascular diseases that cause more death in today’s industrial world. Among the generation of arrhythmias in cardiac myocytes, Early Afterdepolarization (EAD) and Delayed Afterdepolarization (DAD) is most significant one. Sodium -Calcium Exchanger (Na+- Ca2+ X) dysfunction is one of major source of DAD and EAD. Na+- Ca2+ X which exact mechanism is responsible for promoting EAD and DAD still not derived clearly from any cardiac models investigation. It is very important to understand the electrophysiological characteristics of Na+- Ca2+ X and its role in cardiac arrhythmias to clearly detect such arrhythmias effects. In this research article the aim is to build a strong fundamental foundation of Na+- Ca2+ X mechanism in terms of electrophysiological molecular segment (internal structure) arrangements and various Na+- Ca2+ X investigations on cardiac arrhythmias. Na+-Ca2+X is one which belongs to low chemical attraction, high transport capacity and energetically driven by the Na+ ions. The second is an L-type Ca2+ channel, which has a high affinity to Ca2+. Na+-Ca2+X eject nearly thirty (30%) of Ca2+ is required to activate the myofilaments in rabbit, guinea pig and human ventricles and a very small amount (7%) of Ca2+ is required in rat and mouse ventricles. Na+-Ca2+X transport Ca2+ up to 5000 per second (≈6μM/L), which is much greater than SR Ca2+ ATP Ca2+ transport (100 to 150 per second at ≈0.3μM/L). By using voltage patch clamp, Na+-Ca2+X current is measured in guinea pig ventricular myocyte, from that density of Na+-Ca2+X is to be found, 250 to 400 Na+-Ca2+X/μm2 . Na+-Ca2+X current (INaCa) at level [Ca2+]o = 0.50mM, Na+-Ca2+X mechanism of Ca2+ ions removal is very quickly, why because Calcium Induced Calcium Release (CICR) process does increase the cytosolic Ca2+ concentration very early. Enhanced activity of Na+-Ca2+X or increased Na+-Ca2+X channel current reduces the Action Potential (AP) and AP Duration (APD), and triggers rapid firing within cardiac pulmonary veins. Minimum intracellular calcium levels in SR is responsible for systolic dysfunction in failure heart. Similarly it increases the inward Na+-Ca2+X current, life threatening arrhythmias like DAD happen by sudden release of calcium in SR. Finally increased or enhanced or hypertrophy conditions of Na+-Ca2+X is produces EAD and DAD.