REGULATION OF PITUITARY ADRENOCORTICOTROPHIC ACTIVITY DURING THE RESPONSE OF THE RAT TO ACUTE STRESS1

Abstract

The admn. of cortical hormone suppressed the enhanced pituitary adrenocorticotrophic activity which otherwise accompanies environmental change (heat, cold), drug admn. (histamine, epinephrine) and bacterial intoxication (injn. of a suspension of killed typhoid organisms). The data may be interpreted to mean that the great variety of non-specific stresses increases pituitary adrenocorticotrophic activity by a common mechanism, namely, by increasing the requirement of the peripheral tissue cells for cortical hormones. The hypophysis responds to the decrease in conc. of cortical hormone in body fluids by increasing the rate of elaboration of trophic hormone. Certain quantitative relationships hold for this regulatory mechanism. First, the degree of inhibition of pituitary adrenocorticotrophic activity is proportional to the amt. of administered cortical hormone. Second, the greater the degree of stress to which the animal is subjected the greater is the amt. of cortical hormone required to inhibit pituitary adrenocorticotrophic activity. These quantitative data may be adequately explained if it is assumed that the rate of elaboration of A.C.T.H. from the pituitary fluctuates by gradual change and according to the requirements of the tissue cells for cortical steroids. Seven-teen-hydroxycorticosterone, 17-hydroxy-ll-dehydrocorticos-terone, corticosterone, desoxycorticosterone and progesterone have been assigned pituitary inhibitory potency ratings of 4, 4, 1, 1/2, and 1/50, respectively. Since pituitary inhibitory potency resides in both the C11 oxygenated and the C11 de-soxy type steroids it is suggested that the steroids act directly on the ant. pituitary rather than indirectly through products of their metabolic activity or their deficiency.