Adrenocorticotrophic Hormone in the Blood of Adrenalectomized Rats

Abstract

IT is well known that stress results in increased activity of the adrenal cortex which is caused by an increased secretion of adrenocorticotrophin by the pituitary gland. However, the exact mechanism which controls the secretion of this hormone is not fully understood. Sayers and Sayers¹ suggested that stress causes an increased utilization of adrenocortical steroids by the peripheral tissues and the resulting low blood level of corticoids acts as a stimulus to the pituitary gland to increase its secretion of adrenocorticotrophin. The Sayers hypothesis received convincing support from the results of the investigations of Taylor, Albert and Sprague², Gemzell, Van Dyke, Tobias and Evans³ and Sydnor and Sayers⁴, who found that animals with adrenocortical insufficiency exhibited a high blood level of adrenocorticotrophin. On the other hand, Barrett and Hodges⁵ were unable to demonstrate any difference in plasma concentrations of adrenocorticotrophin between normal and adrenalectomized rats three, six and twelve days after the removal of the adrenal glands. The explanation of the discrepancy between these results was difficult to find. However, Barrett and Hodges⁵ did not use the conventional technique of Sayers, Sayers and Woodbury⁶ which employs hypophysectomized rats for the bioassay of adrenocorticotrophin, but a modification of the method described by Hodges⁷ in which normal rats pretreated with deoxycorticosterone acetate were used. The possibility exists that the method was not sensitive enough to detect differences between the plasma-levels of adrenocorticotrophin in the normal and adrenalectomized animals or may even have been completely unsatisfactory for the assay of the hormone in blood. Therefore, it seemed essential to repeat and extend the work using hypophysectomized rats for determination of the adrenocorticotrophin.