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

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 mumol 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.