MindMap Gallery cell transmembrane potential
Resting potential (positive outside and negative inside): K balance potential caused by K diffusing outside the membrane through inward rectifying potassium channels to form an inward rectifying potassium current (Ik1); action potential (negative outside and positive inside).
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working cell transmembrane potential (Take ventricular muscle as an example)
resting potential (positive outside and negative inside)
Generally -90~-80mV
The size mainly depends on the K concentration difference between the intracellular and intracellular fluids and the permeability of the membrane to K
K equilibrium potential caused by K diffusion outside the membrane through inward rectifier potassium channels to form inward rectifier potassium current (Ik1)
inwardly rectifying potassium channel
Non-gated ion channels are not controlled by voltage or chemical signals, and membrane potential affects their opening.
Inward rectification: a phenomenon in which the permeability of Ik1 channels to K is reduced due to membrane depolarization.
Participating current: Main K current, sodium background current, pump current
Action potential (negative outside and positive inside)
Issue 0 (rapid depolarization period)
-90mV→ 30mV (1~2ms) Caused by Na internal flow
Phase 0 depolarization mechanism: stimulation → resting potential -90mV → threshold potential -70mV, activation of fast Na channels (fast Na channels can be blocked by tetrodotoxin TTX) → Na regeneration (inactivation starts at 0mV) → and membrane depolarization The positive feedback between polarization causes the membrane to rapidly depolarize to a level close to the Na equilibrium potential in about 1 ms.
Participating current: Mainly sodium inward current (INa), a small amount of T-type calcium current (ICa-T)
Issue 1 (Initial stage of rapid repolarization)
30mV→0mV (10ms) caused by K outflow
Participating current: Mainly instantaneous outward current (Ito), small amount of chlorine current (Icl) Ito can be selectively blocked by the potassium channel blocker 4-aminopyridine (4-AP)
season2 (Slow repolarization period or plateau period)
0mV (100~150ms) is caused by the slow and persistent inflow of Ca2 (the main reason) and the outflow of K
Participating currents: L-type calcium current (ICa-L), inward rectifier potassium current (Ik1), delayed rectifier potassium current (Ik) ICa-L can be affected by the calcium channel blocker verapamil
It is unique to the action potential of cardiomyocytes and participates in the most complex period of ion flow.
Issue 3 (end of rapid repolarization)
0mV→-90mV (100~150ms) caused by K outflow
Participating currents: Mainly delayed rectifier potassium current (Ik), inward rectifier potassium current (Ik1) involved in terminal repolarization Class III antiarrhythmic drugs inhibit Ik
Main part of repolarization
Issue 4 (Complete repolarization phase or resting phase)
At resting potential -90~-80mV
Affecting ions: Na, K, Ca active transport Mechanism: Sodium-potassium pump Na-Ca exchanger (transfer 3 Na, discharge 1 Ca) small calcium pump
The period from the beginning of phase 0 depolarization to the completion of phase 3 depolarization is called the action potential duration, which is about 200~300ms.