The Effects of Hydrostatic Pressure on A₁ Adenosine Receptor Signal Transduction in Brain Membranes of Two Congeneric Marine Fishes

To investigate the effects of deep-sea temperatures and hydrostatic pressures on transmembrane signal transduction, the A₁ adenosine receptor/inhibitory G protein/adenylyl cyclase complex was studied in brain membranes from two congeneric marine fishes that live at different depths. These scorpaenid species, Sebastolobus alascanus and S. altivelis, have been used as a model system to study adaptations to the deep sea. At 5°C and atmospheric pressure the basal adenylyl cyclase activities of the two species are similar. The inhibition of adenylyl cyclase by the A₁ adenosine receptor-specific agonist, N⁶-cyclopentyladenosine (CPA), was dependent on GTP. The IC₅₀ values for inhibition of adenylyl cyclase by CPA were 2.0±1.14μmoll⁻¹ and 1.6±1.06 for S. alascanus and S. altivelis, respectively. The A₁ adenosine receptor antagonist 8-cyclopentyl-1, 3-dipropylxanthine reversed the CPA-induced inhibition of adenylyl cyclase in a concentration-dependent manner. Brain membranes prepared from the Sebastolobus species incubated at 48.1 MPa (0.1 MPa = l atmosphere) and 5°C for 2.5 h did not lose basal adenylyl cyclase activity or sensitivity to inhibition by CPA when assayed at atmospheric pressure. In contrast, rat brain membranes lost 59% of their activity under these conditions. At atmospheric pressure, the K_m values of 2-deoxy-ATP were identical for the Sebastolobus species adenylyl cyclases. Increased pressure increased the K_m values in both species. However, the K_m of 2-deoxy-ATP was less sensitive to pressure for the enzyme from the deeper-living S. altivelis. Basal adenylyl cyclase activity and the inhibitory effect of 100μmoll⁻¹ CPA were assayed at 0.1, 13.7 and 41.2MPa. Increased pressure inhibited basal adenylyl