Cellular Ca²⁺ metabolism

A variety of cellular responses are mediated by changes in the concentration of cytosolic Ca²⁺ (e.g. contraction, secretion, glycogenolysis). Binding of Ca²⁺ induces conformational changes in Ca²⁺-sensitive proteins that modulate their activity. Cells go to great lengths to maintain extremely low (100–200nmol/l) cytosolic Ca²⁺concentrations ([Ca²⁺]_i) in spite of the large electrochemical gradient (10000:1), which favours strongly the influx of Ca²⁺ from the interstitial fluid (1–2mmol/l) (Fig. 3.25.1). Although there is limited buffering of Ca²⁺ by binding to intracellular proteins, cells need to expend energy to extrude Ca²⁺ through the plasma membrane or to sequester it in intracellular vesicular stores. Indeed, total cell [Ca²⁺] can be in the millimolar range when stored Ca²⁺ is taken into account. Extrusion occurs via Ca²⁺-ATPase and Na⁺–Ca²⁺ exchangers in the plasma membrane and sequestration into intracellular vesicular stores via the sarco(endo)plasmic reticulum Ca²⁺-ATPase (SERCA) (Fig. 3.25.1). In the lumen of these stores, the free [Ca²⁺] is buffered by binding to low-affinity Ca²⁺

Stay updated, free articles. Join our Telegram channel

Join