Control of calcium movement in the myocardium

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Abstract
A model for calcium (Ca) movement in the course of excitation-contraction of mammalian myocardium is presented. At physiological levels of [Ca]o between 500–700 μmol Ca/kg wet tissue is bound within the sarcolemmal-glycocalyx—most at anionic phospholipid sites. This Ca feeds two systems responsible for influx—the channel under control of protein phosphorylation and the Na-Ca exchanger regulated by the level of[Na]1. Respiring mitochondria are activated for Ca exchange in the presence of a proton donor (e.g. phosphate, bicarbonate). The sarcoplasmic reticulum (SR) may not be activated at relatively low levels of Ca influx but is activated as the ‘Ca load’ within the cell rises. Basic control of resting membrane Ca permeability resides at two sites—within the glycocalyx where sialic acid plays a role and within the lipid bilayer where phospholipid disruption leads to increased permeability

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