Ectopic alpha-adrenergic mediated accumulation of guanosine 3',5'-monophosphate in isolated adrenocortical carcinoma cells.
In the normal adrenal cell, epinephrine does not activate the rise of either cGMP or cAMP concentrations. In contrast, epinephrine activates the rise of cGMP but not cAMP concentrations in a concentration-dependent manner in isolated adrenocortical carcinoma cells. This effect was duplicated by the alpha-adrenergic agonist, phenylepherine, but was unaffected by the beta-adrenergic agonist, isoproterenol. The epinephrine-activated increase in cGMP was blocked by the alpha-adrenergic antagonist, phentolamine, but was not interfered with by the beta-adrenergic antagonist, propranolol. Neither acetylcholine, a cholinergic agonist, nor exogenous calcium caused any increase in cGMP. The rise of cGMP maximally activated by ACTH was additive with that obtained with epinephrine. These results indicate that the adrenal neoplastic cell possesses ectopic alpha-adrenergic receptors, and that epinephrine causes a rise of the cGMP level through these receptors. The data, furthermore, suggest that the receptors for ACTH and epinephrine are distinct.
D000109:Acetylcholine / Q000494:pharmacology; D000306:Adrenal Cortex Neoplasms / Q000378:metabolism*; D000324:Adrenocorticotropic Hormone / Q000494:pharmacology; D000818:Animals; D001285:Atropine / Q000494:pharmacology; D002460:Cell Line; D000242:Cyclic AMP / Q000378:metabolism; D006152:Cyclic GMP / Q000378:metabolism*; D004305:Dose-Response Relationship, Drug; D004837:Epinephrine / Q000494:pharmacology*; D007545:Isoproterenol / Q000494:pharmacology; D010646:Phentolamine / Q000494:pharmacology; D010656:Phenylephrine / Q000494:pharmacology; D011433:Propranolol / Q000494:pharmacology; D051381:Rats
D010656:Phenylephrine; D001285:Atropine; D000324:Adrenocorticotropic Hormone; D011433:Propranolol; D000242:Cyclic AMP; D006152:Cyclic GMP; D007545:Isoproterenol; D000109:Acetylcholine; D004837:Epinephrine; D010646:Phentolamine