Affiliations: University Laboratory of Physiology, Oxford University, Parks Rd, Oxford OX1 3PT, UK
Note: [] Address for correspondence: Dr J. Urban, Physiology Laboratory, Oxford University, Parks Rd, Oxford OX1 3PT, UK. Tel.: +44 18965 272509; Fax: +44 1865 272469; E‐mail: jpgu@physiol.ox.ac.uk.
Abstract: The intracellular milieu of chondroctyes is regulated by an array of proteins in the cell membrane which operate as transport pathways, allowing ions and nutrients such as glucose and amino acids and metabolites such as lactate to cross the plasma membrane. Here we investigated the influence of hydrostatic pressure on intracellular calcium concentrations ([Ca2+]i) in isolated bovine articular chondrocytes. We found that short applications of high hydrostatic pressures led to a significant increase in [Ca2+]i. The pressure‐induced rise was abolished for long (240 sec) but not short (30 sec) pressure applications by removal of extracellular Ca2+. The rise in pressure was also blocked by the inhibitors neomycin and thapsigargin confirming that pressure, by generating IP3, led to an increase in [Ca2+]i by mobilising the pool of Ca2+ ions contained within intracellular stores. We also found that intracellular [Na+] was affected by a rise in osmotic pressure and further affected by application of hydrostatic pressure. The effect of hydrostatic pressure on sulphate incorporation depended strongly on extracellular osmolality. Since significant gradients in extracellular osmolality exist across intact cartilage, the results imply that responses of chondrocytes to the same pressure will vary depending on location in the joint. The results also indicate that hydrostatic pressures can affect several different transporter systems thus influencing the intracellular milieu and chondrocyte metabolism.
Keywords: Calcium, sodium pump, mechanotransduction, ion transport, osmotic pressure
Journal: Biorheology, vol. 41, no. 3-4, pp. 299-308, 2004
