Ions are Freed from Electrostatic Restraint by Depolarisation

Literature Review

Abstract

We recalled the work of Langer in the 1980s showing calcium ions bound to the inner leaflet of cardiac sarcolemma in diastole, which detaches during depolarisation into the cytoplasm. We postulate that this and some unbound calcium ions comprise the calcium that triggers calcium ion release from the sarcoplasmic reticulum, causing contraction. Also during depolarisation, potassium ions are extruded from the sinus node cells into the extracellular fluid. Neither of these actions involve crossing a barrier and therefore do not need channels or “gates”. The ions simply flow down their concentration gradients. Here, an alternative hypothesis is presented, that draws attention to the resting electric field force, equal to the trans-membrane potential, divided by the membrane thickness of about 5nm, an electric field force of the order of 107Vper metre. Depolarisation to a transmembrane potential of zero was demonstrated in sinus node cells; reducing the electric field strength also to zero frees the ions from electric restraint. Freed ions cannot move against their concentration gradient. Sodium is pumped out using up ATP energy; calcium is pumped out of the sarcoplasmic reticulum by a calcium activated ATPase and out of the cell by the sodium-calcium exchange (NCX). Langer thought sarcolemmal calcium was involved in the NCX. We postulate that the potassium ions extruded by cardiac cells during action potentials must be quantitatively equal to those entering the cell during sodium pumping.