Sheep with exteriorized cervical adrenal autotransplants were used to study the dynamics of cyclic adenosine 3',5'-monophosphate (cAMP) release into adrenal venous (A-V) blood during local adrenal stimulation of cortisol (F) and aldosterone secretion. When F secretion was basal (<0.1 μg/min), A-V cAMP concentration was equal to peripheral plasma levels of 12–25 nM. Large doses of ACTH (1.6–166 mU/min) sufficient to produce maximum F secretion caused brisk increases (5–25-fold) in cAMP release without changing peripheral plasma cAMP concentration. Doses of ACTH causing submaximal F secretion (0.04–0.16 mU/min) did not stimulate cAMP release and angiotensin (0.16 μg/min) and potassium (21–24 /mioles/min) although producing maximum aldosterone secretion, also failed to increase release. With the onset of ACTH stimulation (16.6–166 mU/min), change in cAMP concentration above basal levels preceded change in F by at least 1 min and cAMP release rates fell more promptly than F secretion following cessation of ACTH stimulation. During massive and prolonged ACTH stimulation, a decline in cAMP release after 40 min was observed despite continuing ACTH stimulation and maximum F secretion, and peak release rates were not restored with the concurrent infusion of aminophylline. Aminophylline alone (2.7 mg/min) stimulated both F and cAMP release although ACTH mediated cAMP increases were not greatly augmented during combined infusions. Prolonged dexamethasone pretreatment, sufficient to markedly reduce and delay F response to ACTH, did not affect cAMP release. These physiologic studies, showing similar patterns to previous work in vitro, indicate that release is closely coupled to cAMP formation. (Endocrinology95: 838, 1974).
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Espiner et al. (1974) studied this question.