THE EFFECT OF ACUTE AND CHRONIC DESOXYCORTICOSTERONE ACETATE PRETRE’ATMENT ON THE PITUITARY-ADRENAL RESPONSE TO STRESS¹

The Effect of Desoxycorticosterone Acetate on the Release of Adrenocorticotrophin by the Pituitary Gland

“…It is probable that Gershberg et al (1950) were unsuccessful in demonstrating the pituitary inhibitory effect of DOCA, since they subjected their rats to stress too soon after the subcutaneous administration of the steroid. It is more difficult to explain the discrepancies which exist between the results obtained in the present work and those of Hall et al (1951) and Moya and Selye (1948).…”

“…However, it was found that the doses of DOCA required to prevent the increased secretion of ACTH, in response to the stress of ether anaesthesia and unilateral adrenalectomy, were fifty to one hundred times as great as those which Sayers and Sayers (1947) (1948), Hall et al (1951), and Gershberg et al (1950). It is probable that Gershberg et al (1950) were unsuccessful in demonstrating the pituitary inhibitory effect of DOCA, since they subjected their rats to stress too soon after the subcutaneous administration of the steroid.…”

“…They suggested that, in severe stress, the secretion of adrenocorticotrophic hormone is controlled by a mechanism which the " peripheral-humoral " theory fails to explain. Hall, Finerty, Hall, and Hess (1951) found that desoxycorticosterone acetate administered acutely (24 mg. per 80-100 g. rat intraperitoneally in vegetable oil) or chronically (50 mg. per 80-100 g. rat subcutaneously as pellets) caused no adrenal ascorbic acid depletion. They reported that these large doses of DOCA failed to prevent the fall in adrenal ascorbic acid concentration caused by the stress of scalding.…”

“…However, Moya and Selye (1948), Hall, Finerty, Hall, and Hess (1951), and Gershberg, Fry, Brobeck, and Long (1950 did not find that DOCA prevents the release of ACTH in response to stress.…”

The Quantitative Assay of Corticotrophin Using Rats Treated With Hydrocortisone Acetate

“…Sayers and Sayers (1947) were the first to suggest that several crystalline cortical steroids, including cortisone, hydrocortisone and deoxycortone, were most effective in blocking release of corticotrophin from the pituitary. Casentini, De Poli, Hukovic and Martini (1957), in a comparative test of the relative potencies of various corticosteroid preparations, found that deoxycortone had about the same activity as hydrocortisone acetate in a test on unilaterally adrenalectomized rats (Abelson and Baron, 1952;Porter and Jones, 1956).On the other hand, Fortier, Yrarrazaval and Selye (1951) showed that both cortisone and cortisone acetate were completely ineffective in preventing the release of pituitary corticotrophin in response to stress, and Moya and Selye (1948), Gershberg, Fry, Brobeck and Long (1950) and Hall, Finerty, Hall and Hess (1951) were unable to confirm that deoxycortone acetate had an D inhibitory effect under similar conditions. Hodges (1953, 1954) found that rats were far more suitable for a quantitative assay after treatment with deoxycortone acetate than after cortisone acetate, but even larger doses of deoxycortone failed to give a satisfactory preparation.…”