Ectopic α-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 α-adrenergic agonist, phenylepherine, but was unaffected by the β-adrenergic agonist, isoproterenol. The epinephrine-activated increase in cGMP was blocked by the α-adrenergic antagonist, phentolamine, but was not interfered with by the β-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 posseses ectopic α-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. (Endocrinology106: 1589, 1980)