Role of ion Regulation in Heartbeat Initiation

Abstract

The heart can beat quite 2 billion times in normal life, but the mechanism by which the guts beats is that the subject of intense research. Since the invention of pacemaker currents in 1978, several studies have shown that rhythmic changes in membrane tension (the "membrane tension clock") underlie the mechanism of automation. It's the depolarizing current activated during hyperpolarization. Therefore, when the guts cells recover, it's activated, the cell wall slowly depolarizes, and action potentials begin. However, recent studies have shown that the rise in intracellular Ca (Ca (i)) induced by spontaneous rhythmic sarcoplasmic reticulum Ca release (“calcium clock”) is additionally involved within the initiation of a heartbeat. The elevated Ca (i) activates another ionic current (sodium-calcium exchange current, or I (NCX)), causing spontaneous phase 4 depolarization. Under normal conditions, both clocks are required to trigger a heartbeat. Clock dysfunction is related to sinus node dysfunction in coronary failure and fibrillation. Further research is required to work out how both watches work together to initiate a heartbeat in normal and illness. The guts can beat quite 2 billion times in normal life, but the mechanism by which the guts beats is that the subject of intense research. Since the invention of pacemaker currents (If) in 1978, several studies have shown that rhythmic changes in membrane tension (the "membrane tension clock") underlie the mechanism of automation. It is that the depolarizing current that's activated during hyperpolarization. Therefore, when the guts cells recover, If is activated, the cell wall slowly depolarizes, and action potentials begin. However, recent studies have shown that spontaneous and rhythmic sarcoplasmic reticulum Ca release (“calcium clock”)-induced increase in intracellular Ca (Cai) is additionally involved within the initiation of a heartbeat increase. the rise in chi activates another ionic current (sodium-calcium exchange current, or INCX), which causes spontaneous phase 4 depolarization. Under normal conditions, both clocks are required to trigger a heartbeat. Clock dysfunction is related to sinus node dysfunction in coronary failure and fibrillation. Further research is required to work out how both watches work together to initiate a heartbeat in normal and illness.