HEPATIC REGULATION OF ADRENAL CORTICAL FUNCTION12

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Abstract
Under many different experimental and physiological conditions, a close correlation has been found between the size of the adrenal glands and the ca-pacity of the liver to inactivate adrenal cortical hormones by ring A reduction in vitro. We have concluded from this close correlation that there is a similar parallel relationship between the in vivo capacity of the liver to inactivate corti-costeroids, and the adrenal cortical secretion rate. This conclusion is based on several assumptions which are discussed. The present experiments demon-strate that this relationship denotes secondary responses of the adrenal cortex to primary, independent variations in hepatic inactivation of corti-costeroids. Neither ACTH nor adrenal cortical hormones increases the capacity of the liver to inactivate corticosteroids. In contrast, however, a primary diminution of hepatic capacit for adrenal steroid inactivation by surgical removal of 65% of the liver tissue can cause secondary adrenal atrophy. Therefore, the parallel relationship between hepatic capacity for inactivation of adrenal cortical hor-mones by ring A reduction, and the size of the adrenal glands represents a con-trolling influence of the liver on adrenal cortical function, rather than the reverse. This hepatic regulation of adrenal cortical function is apparently mediated through the anterior pituitary (ACTH) negative-feedback control which stabilizes plasma corticosteroid concentration. Our data indicate that the con-trol very effectivey matches the mean input of adrenal cortical hormones to any given output over wide ranges of steroid inactivation rates. By means of these data, the automatic control properties of the hepatic-anterior pituitary-adrenal cortical system are analyzed to show that the amount of TPNH-bound Δ4-steroid hydrogenases in the liver may affect: a) the time constant of the system (the time required to diminish by 63% a deviation from the mean plasma corticosteroid concentration); b) the extent of hunting of plasma corticosteroid concentration about a mean value; c) the half-life of the steroid molecules in the system; d) the velocity of their inactivation at any given plasma corticosteroid concentration; and, e) the mean concentration of adrenal cortical hormones in the blood.