Differential effects of hydrostatic pressure on cation transport pathways of isolated articular chondrocytes.J Cell Physiol. 1999 Feb; 178(2):197-204.JC
Articular cartilages are exposed to significant loads in vivo, which by their effects on chondrocyte metabolism can alter the mechanical properties of the extracellular matrix. The mechanism(s) by which chondrocytes sense and respond to load are not well understood. One component of load, hydrostatic pressure, can be studied independently of the other factors that change during load. In this study, the effects of pressure have been investigated on three K transport pathways in isolated bovine articular chondrocytes. Pressure inhibited the Na/K pump (ouabain-sensitive), Na/K/2Cl cotransporter (bumetanide-sensitive), and residual (ouabain- and bumetanide-insensitive) pathways; however, the response of each system was different. Both pressure level and duration were important in determining the extent of inhibition. There was marked suppression of the Na/K pump, particularly when pressure (2.5-50 MPa) was maintained for the full incubation period (usually 10 min). The Na/K/2Cl cotransporter was more pressure-sensitive, with only a short application (20 sec) of a low pressure (7.5 MPa) being sufficient for inhibition. Over the higher range (20-50 MPa), pressure had little further effect. The inhibitory action on the Na/K pump was dependent on the [Na]i. Thus, when the [Na]i was set to values above or below those normally present, the inhibitory effect was reduced or abolished. The suppressive effect of pressure on Na/K pump and residual pathways was reversed at atmospheric pressure. The pressure dependence of inhibition of the K flux through the residual pathway was similar to that reported for lipid bilayers. These results indicate that hydrostatic pressure may act directly on chondrocyte membrane transporters. Alterations to matrix synthesis resulting from the application of load might therefore result in part from variations to the intracellular ionic/osmotic composition of chondrocytes arising from changes to the activity of membrane transport pathways.