RESPONSE OF PLASMA-MEMBRANE TO APPLIED HYDROSTATIC-PRESSURE IN CHONDROCYTES AND FIBROBLASTS

Effects of applied hydrostatic pressure on transmembrane potentials were investigated in sheep articular chondrocytes and human skin fibroblasts in non-confluent monolayer cultures. Resting potentials in chondrocytes (about -12 mv) and in fibroblasts (about -15 mV) were increased and decreased respectively by over 40% after pressure was applied cyclically (0.33 Hz, 120 mm Hg, 20 minutes). Continuous pressure (120 mm Hg, 20 minutes) caused deplorization in both cell types. Low frequency pressure application (< 0.08 Hz) caused depolarization in chondrocytes and hyperpolarization in fibroblasts. Quinidine (2 × 10-5M) blocked and verapamil (10-5M) reduced hyperpolarization responses, suggesting involvement of Ca2+-dependent K+channels. A23187 (1.9 × 10-6M) caused hyperpolarization in chondrocytes, augmented further by subsequent pressure application (0.33 Hz). Tetrodotoxin (10-6M) blocked depolarization responses indicating that these were due to Na+influx. Blockade of histamine H1 receptors by chlorpheniramine maleate (5.1 × 10-6M), H2 receptors by cimetidine (7.9 × 10-6M) and βadrenoreceptors by sotolol (1.3 × 10-4M) had no effect on hydrostatic pressure-induced hyperpolarization in chondrocytes. Cytochalasin B (2 × 10-5M and at 4 × 10-6M) abolished pressure-induced hyperpolarization in chondrocytes; in contrast, applied cyclical hydrostatic pressure to cytochalasin-treated fibroblasts caused hyper-polarization, suggesting that cytoskeletal changes were involved. © 1992 Informa UK Ltd All rights reserved: reproduction in whole or part not permitted.