title: Inhibition of beta-adrenergic responsiveness in muscle cell cultures by dexamethasone.
abstract: Cultures of two myogenic cell lines, L6E9 and L8, were grown in the absence or presence of dexamethasone. Dexamethasone (1 microM) completely inhibited the formation of myotubes. Partial inhibition (20-40%) was obtained at a concentration as low as 1 nM. Dexamethasone also inhibited beta-adrenergic responsiveness, as noted by decreases in isoproterenol-stimulated adenylate cyclase activity and cAMP accumulation. These effects were both dose and time dependent. In the presence of dexamethasone, the number of beta-adrenergic receptors, as assessed by [125I]iodohydroxybenzylpindolol binding, decreased coordinately with the decrease in cAMP. A high affinity, limited capacity cytosolic binding site for [3H]triamcinolone acetonide observed under control conditions (Kd = 0.7 nM; maximum binding, 2.7 pmol/mg protein) increased in number as a function of developmental state. These data indicate that glucocorticoids inhibit myogenesis and beta-adrenergic responsiveness in vitro.
mesh_terms: D000262:Adenylyl Cyclases / Q000378:metabolism; D000818:Animals; D002459:Cell Fusion / Q000187:drug effects; D002460:Cell Line; D000242:Cyclic AMP / Q000378:metabolism; D003600:Cytosol / Q000378:metabolism; D003907:Dexamethasone / Q000494:pharmacology*; D007700:Kinetics; D009132:Muscles / Q000378:metabolism*; D010869:Pindolol / Q000031:analogs & derivatives / Q000378:metabolism; D051381:Rats; D011941:Receptors, Adrenergic / Q000378:metabolism*; D011943:Receptors, Adrenergic, beta / Q000187:drug effects / Q000378:metabolism*; D011965:Receptors, Glucocorticoid / Q000378:metabolism; D014222:Triamcinolone Acetonide / Q000378:metabolism
chemical_list: D011941:Receptors, Adrenergic; D011943:Receptors, Adrenergic, beta; D011965:Receptors, Glucocorticoid; C011878:iodohydroxybenzylpindolol; D003907:Dexamethasone; D010869:Pindolol; D000242:Cyclic AMP; D000262:Adenylyl Cyclases; D014222:Triamcinolone Acetonide