Resting membrane potential

1.Resting membrane potential(RMP)#

• =(Conductance占全conductance的比例)*(each electrolyte的Equilibration potentials)的總和
  • E(RMP)=[C(Na)/C(total)]*E(Na) + [C(K)/C(total)]*E(K) + [C(Ca)/C(total)]*E(Ca) + [C(Cl)/C(total)]*E(Cl) + ....
    • E=平衡電位
    • 正常情況K ~ -90 mV, Cl ~ -70 mV, Na ~ +60 mV, Ca ~ +125 mV; 但主要conductance為K(靜止時由 leak K+ channels/Kir/K2P 絕對主導, Cl− 次之), Na conductance低, Ca conductance幾乎為0, 所以E(RMP)為-70~-80mV
      • 雖然Ca conductance為0導致高低血鈣不影響Resting potential, 但是Ca有small affinity for Na channels and can essentially "plug" it up during the influx of Na, 所以hypercalcemia會decrease neurons transmitting impulses-->muscle weakness, constipation
      • 而hyperkalemia電生理具二相性：初期細胞外鉀↑使靜止膜電位向 0 mV 偏移(less negative, 如 -90 移至 -75 mV)靠近閾值，興奮性短暫增加(肌束顫動)；然而持續去極化使電壓閘門鈉通道(voltage-gated Na channels)之去活化閘門(h-gates)關閉進入去活化狀態(inactivated state)，鈉通道無法重置，動作電位上升速率(Vmax)驟降，膜進入完全不可興奮狀態(inexcitable) $\to$ 導致弛緩性麻痺(flaccid paralysis)與心臟傳導阻滯
        • 相反hypokalemia會導致more negative membrane potential(hyperpolarized)-->decrease membrane excitability-->weakness/paralysis(However, in some cardiac cells (such as Purkinje fibers), hypokalemia causes K2P1 channels, which are normally selective for potassium, to transport sodium into the cells, causing depolarization. This leads to increased membrane excitability and arrhythmias)
      • Hypernatremia-->DTR↑(注意:RMP由K+通透性主導，靜止時鈉通透性僅鉀的 1/100，血鈉變化對 RMP 貢獻趨近於零；臨床 DTR↑/易激動/seizure 主因是高滲透壓引發腦細胞脫水與神經元收縮)
        • 相反Hyponatremia-->DTR↓(主因腦細胞低滲透壓水腫與中樞抑制，非 RMP 直接位移)