Abstract
ACTH concentrations in the pituitary glands of normal rats remain unchanged 2.5 min after sham adrenalectomy, a time at which ACTH concentrations in the blood are known to reach a maximum. Four hr later, the ACTH concentration in the gland is about half that of unstressed control animals. A second similar stress applied at this time results in a similar release of ACTH into the blood at 2.5 min, but the pituitary now shows a 2-fold increase in ACTH concentration. Similar increases in pituitary ACTH concentrations occur 2.5 min following the stress of ether anesthesia 8 hr after the stress of adrenalectomy. Rats adrenalectomized 30 days show an elevated circulating ACTH level and a pituitary ACTH concentration 3 times that of normal animals; this pituitary concentration is doubled 2.5 min after ether stress. In contrast with normal animals, rats, 5, 10, 20 or 30 days after adrenalectomy, do not show a decrease in pituitary ACTH content 160 min after stress. A single “blocking” dose of hydrocortisone prevents both the release and the increase in pituitary ACTH content after stress but has no effect on the resting level in the gland. It is suggested that the ability of the adenohypophysis to release ACTH after stress is independent of the prestress pituitary concentration but rather depends on the ability of the gland to synthesize “new” ACTH rapidly.