How heart is working in Tamil science behind heart cells

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#myocytes • #purkaji • #conductionststem • #pacemaker • #pstamil • #high_bp • #actionpotential • #tamil • • calcium, action, potential, depolarization, repolarization, cardiac, systole, contraction, ions, gradients, membrane, potassium, sodium, fast, muscle, yt:quality=high, cardiology lectures, cardiac action potential, action potential in pacemaker cell, action potential in contractile myocytes, physiology of the heart, heart muscle, electrophysiology, cardiac myocytes, SA node action potential, gap junctions, membrane potential, funny currents, voltage-gated ion channels, funny channels, pacemaker potential, • av node, sa node, system, conduction, electrical, pacemaker, explained, process, anatomy and physiology, intrinsic cardiac conduction system, ecg interpretation, cardiac physiology, usmle, medical lectures, medical education, cardiomyocytes action potential, cardiomyocytes, heart cells, ninja nerd lectures, action potential in heart, cardiac muscle, ventricular action potential, action potential animation, myocardial action potential animation, slow phase 4, phase 1, phase 0, myocytes, cardiac muscles, action potential., • • Physiology, Action Potential • Grider MH, Jessu R, Kabir R. • Publication Details • Introduction • An action potential is a rapid sequence of changes in the voltage across a membrane. The membrane voltage, or potential, is determined at any time by the relative ratio of ions, extracellular to intracellular, and the permeability of each ion. In neurons, the rapid rise in potential, depolarization, is an all-or-nothing event that is initiated by the opening of sodium ion channels within the plasma membrane. The subsequent return to resting potential, repolarization, is mediated by the opening of potassium ion channels. To reestablish the appropriate balance of ions, an ATP-driven pump (Na/K-ATPase) induces movement of sodium ions out of the cell and potassium ions into the cell. • Cellular Level • Although usually discussed in the context of neuronal cells, action potentials also occur in many excitable cells such as cardiac muscle and some endocrine cells.[1][2] Within a population of neurons, there can be significant variability in the intrinsic electrical properties of the cell, such as resting potential, maximum firing rate, resistance to current, and width of action potentials. These variables are directly dependent upon the number, location, and kinetics of ion channels within the membrane.[3] • Within the heart, pacemaker cells located in the SA node initiate action potentials intrinsically and rhythmically. Unlike in neurons, the majority of current in pacemaker cells gets mediated through calcium flux. A transient current of calcium ions, mediated by T-type calcium channels, slowly depolarizes the pacemaker cell until reaching the threshold potential for L-type voltage-gated calcium channels, inducing an action potential.[4] The action potential is then dispersed throughout the heart by myocardiocytes, cardiac muscle cells that contract while they conduct the current to neighboring cells. Similar to action potential initiation in neurons, and in contrast to pacemaker cells, myocardiocytes initiate rapid depolarization through voltage-gated sodium channels.[1] • • Function • A neuronal action potential has three main stages: depolarization, repolarization, and hyperpolarization. The initial depolarization is determined by the cell’s threshold voltage, the membrane potential at which voltage-gated sodium channels (Nav) open to allow an influx of sodium ions. The flow of positive sodium ions into the cell leads to further depolarization of the membrane, thus opening more Nav in a positive-feedback loop. Depolarization in mature neurons lasts approximately 1 msec, at which time the Nav are inactivated and no longer able to flux ions.[10] • Repolarization begins as voltage-gated potassium channels (Kv) open. Although Kv have approximately the same threshold voltage as Na, the kinetics of the potassium channel are much slower. Therefore, after approximately 1 msec, there is an opening of the slower Kv channels that is coincident with the inactivation of the faster Nav channels. The flow of potassium ions out of the cell results in a decrease in membrane potential towards the cell’s resting voltage. When the membrane potential falls below the threshold, both the Nav and the Kv begin to close. However, the Kv have slow kinetics and remain open slightly longer than needed to return the cell to resting membrane voltage. The brief dip in the membrane potential below the normal resting voltage is termed hyperpolarization.

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