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Adenyl cyclase activity resulting in increased 3'5' cyclic adenosine monophosphate (AMP) formation can be stimulated by vasopressin (ADH), corticotrophin (ACTH), and adrenaline in various tissues (Sutherland & Rall, 1960). Cyclic AMP has been postulated as an intermediate in the stimulation of adrenal cortical secretion by ACTH and vasopressin (Hilton, Scian, Westermann, Nakano & Kreusi, 1960).

Northrup & Parks (1964) and Davoren & Sutherland (1963) have recently shown that stimulation of adenyl cyclase activity by adrenaline can be inhibited by the receptor blocking agent, dichloroisoproterenol (DCI). Northrup & Parks (1964) have shown also that dihydroergotamine (DHE) inhibits cyclic AMP action in the liver. Thus it is possible to interfere with the adenyl-cyclic AMP system at two different stages: in the formation of cyclic AMP by DCI and by the inhibition of cyclic AMP with DHE. The influences of DHE and DCI on steroid synthesis in the adrenal cortex alone and in