Effect of Estrogen Administration on Extravascular Cortisol

Abstract

Analyses of arterial-blood radioactive-cortisol disappearance curves in human subjects by means of 2-compartment mathematical models have provided data on extravascular and intravascular cortisol. The intravascular cortisol pool is 460 [plus or minus] 209 SD fg distributed in a volume equal to plasma volume. Extravascular cortisol is or 3 times as largely distributed in an unknown volume. Estrogen treatment causes a marked increase in intravascular cortisol without significant effect on extravascular cortisol. This is in contrast to ACTH stimulation, which causes proportional increases in both pools. Kinetic processes are changed by estrogen treatment with a resultant tendency for cortisol to remain in the intravascular pool. These data, taken in conjunction with the previously observed lack of hypercorticism in estrogen-treated subjects, are consistent with the hypothesis that it is the extravascular cortisol which is physiologically active. They indicate that a function of transcortin is to maintain a large intravascular pool of cortisol which is not readily available for catabolism.