Release of corticosterone from the rat adrenal cortex in response to administration of (1–24)adrenocorticotrophin

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Abstract
The intraperitoneal injection of (1–24)ACTH (34–170 nmol/kg) in rats pretreated with betamethasone resulted in a biphasic rise in plasma corticosterone; only a single phase-response was observed after lower doses (3·4–17·0 nmol/kg). There was an initial rapid rise to a level of approximately 0·72 μmol corticosterone/l plasma over the first 10 min after injection, followed by a plateau phase in which there was no further significant rise in steroid levels up to 25 min. Between 25 and 30 min after injection there was a second significant rise in plasma corticosterone concentration. The amplitude of the first phase of steroid increase was essentially the same for all doses of (1–24)ACTH administered whereas the amplitude of the second phase was dose-dependent. The administration of the microtubule inhibitor, colchicine, greatly reduced the amplitude of the second phase of the response to (1–24)ACTH while not affecting the first phase. However, a second stimulus with (1–24)ACTH in colchicine-treated animals was without effect on plasma corticosterone concentrations; both the first and second phases of corticosteroid increase being abolished. It is proposed that the first phase of plasma corticosterone increase resulted from the release of corticosteroid from a storage form close to the cell membrane and not requiring microtubular transport, whereas the second phase was the result of transport from more distant storage sites or de-novo synthesis.