explain the significance of k+ in establishing resting membrane potential
Resting potential For most animal cells potassium ions (K+) are the most important for the resting potential.[1] Due to the active transport of potassium ions, the concentration of potassium is higher inside cells than outside. Most cells have potassium-selective ion channel proteins that remain open all the time. There will be net movement of positively charged potassium ions through these potassium channels with a resulting accumulation of excess negative charge inside of the cell. The outward movement of positively charged potassium ions is due to random molecular motion (diffusion) and continues until enough excess negative charge accumulates inside the cell to form a membrane potential which can balance the difference in concentration of potassium between inside and outside the cell. "Balance" means that the electrical force (potential) that results from the build-up of ionic charge, and which impedes outward diffusion, increases until it is equal in magnitude but opposite in direction to the tendency for outward diffusive movement of potassium. This balance point is an equilibrium potential as the net transmembrane flux (or current) of K+ is zero. A good approximation for the equilibrium potential of a given ion only needs the concentrations on either side of the membrane and the temperature. It can be calculated using the Nernst equation:
Cardiac action potential This phase is also known as the "plateau" phase due to the membrane potential remaining almost constant, as the membrane very, very slowly begins to repolarize. This is due to the near balance of charge moving into and out of the cell. During this phase delayed rectifier potassium channels allow potassium to leave the cell whilst L-type calcium channels (activated by the flow of sodium during phase 0), allow the movement of calcium into the cell. This calcium, binds to and opens more calcium channels (called ryanodine receptors) located on the sarcoplasmic reticulum within the cell, allowing the flow of calcium out of the SR. This calcium is responsible for contraction of the heart. Not only that, but it also activates chloride channels called Ito2, which allow Cl− to enter the cell. Together the movement of both Ca2+ and Cl− oppose the voltage change caused by K+. As well as this the increased calcium concentration increases the activity of the sodium-calcium exchanger, and the increase in sodium entering the cell increases activity of the sodium-potassium pump. The movement of all of these ions results in the membrane potential remaining relatively constant.[17][8] This phase is responsible for the large duration of the action potential and is important in preventing irregular heartbeat (cardiac arrhythmia).