The Effects of High Pressure on Signal Transducing Systems of Cultural Endothelial Cells

Abstract

To investigate the involvement of Ca-mobilizing signal transduction in cell modifications at high pressure we used well known Ca- agonists - histamine, serotonin and bradikinine. Besides human umbilical EC, cultured smooth muscle cells (SMC) and bull pulmonary artery endothelial cells (BPAEC) were used. It was shown that neither histamine (10-5 M), nor serotonin (l0-6M) stimulated PI-turnover after 30 min exposure to 6 MPa high hydrostatic pressure (HHP). The basal level of IPn did not differ from control cells. Similar results were obtained in cultured SMC (disappearance of serotonin stimulation) and in cultured BPAEC (disappearance of bradikinine stimulation). Thus, this pressure had no influence on basal Pl-turnover but inhibited membrane signal transduction. 10 MPa HHP increased the all fraction of IPn (IP1, IP2, IP3) up to 135%, but histamine did not activate the Ca-mobilising system in human EC after decompression in concentration more than 10 times higher than that usually used for activation control cells. To compare the effects of HHP and high partial pressure of nitrogen and helium we studied Pl-turnover in EC after fast decompression. In case of human EC HHP and high partial pressure of N2 and He did not have an effect on IPn basal level, but signal transduction trough Pl-turnover was inhibited. Activation «R - G-pr. - PL C» complex was observed only after slow decompression or after 30-60 min incubation at normal pressure. These results suggest the desensitisation of EC during HHP exposure.