The SCN5A protein winds through the membrane of heart muscle cells, forming a channel that opens to let
sodium ions flow into the cells.
When appropriately stimulated, the channels open,
sodium ions flow in, and the muscle cells contract.
Drugs that specifically target the persistent
sodium ion flow, or current, have been approved by the Food and Drug Administration for treating epilepsy.
Not exact matches
Bound to the cell membrane, Na ± K+ATP ase uses the energy of adenosine triphosphate (ATP) molecules to pump
sodium out of the cell and potassium into the cell, maintaining a charge gradient that allows
ions to
flow through open channels.
When you stimulate a neuron,
ions like
sodium and potassium and chloride
flow back and forth, causing what's called an action potential to travel down the neuron, through the axon, to a synapse.
In this scenario, when an object moved in the neuron's preferred direction, excitatory impulses would reach the target neuron first, triggering positively charged
sodium ions to
flow into the cell — an excitatory current.
According to a research team led by Thomas Hund, the key may reside in voltage-gated
sodium channels, nanoscopic pores that control the
flow of
sodium ions across the heart cell membrane.
Like a type of door,
sodium channels allow
sodium ions to
flow into nerve cells through tiny pores.
For example, if a magnetic field is strong enough to attract or repel
ions such as
sodium and chloride in the blood, these
ions may eventually encounter the walls of the blood vessels, move more rapidly, and cause an increase in tissue temperature or an increase in blood
flow.
Lactic acid counters this fatigue by interfering with the
flow of chlorine
ions - effectively lowering the amount of
sodium current necessary for muscle activation.