Receptor availability defines the extent of agonist-mediated G-protein down-regulation in neuroblastoma × glioma hybrid cells transfected to express the β2-adrenoceptor

AbstractSustained exposure of neuroblastoma × glioma hybrid, NG108-15, cells transfected to express the human, β2-adrenoceptor (clone βN22) to isoprenaline or iloprost (an agonist at the endogenously expressed IP prostanoid receptor) resulted in a substantial and selective down-regulation of the α subunit of the G-protein Gs. Treatment of these cells with the irreversible β-adrenoceptor antagonist bromoacetyl alprenolol menthane diminished both the potency and the maximal ability of isoprenaline but not of iloprost to cause Gsα down-regulation. These results demonstrate that the extent of agonist-mediated Gsα down-regulation is dependent upon the availability of receptor to agonist