INVESTIGATION OF THE RELEASE OF ACTH1

Abstract

The ACTH-releasing activity of portal vessel plasma, as estimated by adrenal ascorbic acid depletion in the steroid-depressed rat, was present in protein fraction III₀. The reduction in adrenal ascorbic acid concentration following injection of III₀ was not attributable to the presence of ACTH in this protein fraction since III0 was inactive in the hypophysectomized rat. The remaining protein fractions had no significant effect on adrenal ascorbic acid concentration. The activity attributable to III₀ was lost during dialysis when the protein fraction was dissolved in a buffer solution containing 15.2% ethanol. This suggested either destruction of the active component or dissociation of a dialyzable component from the carrier protein. Fraction III₀ from carotid artery plasma was inactive regardless of whether the blood was collected rapidly, slowly, or allowed to remain mixed with macerated skeletal muscle for two hours at 0° C. The ACTH-releasing activity of portal plasma III₀ was not attributable to contamination with nor-epinephrine, epinephrine, histamine, or serotonin. Similarly, injection of NaCl solutions of different concentrations were ineffective.