Hepatic estrogen receptors were measured in ovariectomized female rats using isoelectric focusing in polyacrylamide gel. Hypophysectomy or adrenalectomy reduced the receptor level to approximately 10% and 42%, respectively, of the control value. Treatment of hypophysectomized (Hx) rats with dexamethasone alone was without effect. When Hx rats were given a pituitary transplant under the kidney capsule in order to induce liver estrogen receptors, dexamethasone treatment more than doubled the inductive effect of the pituitary transplant. The administration of human GH (hGH) in osmotic minipumps to Hx rats led to an induction of hepatic estrogen receptor levels to 48% of the control value. When hGH infusion was combined with dexamethasone treatment, a complete restoration of the receptor level to that in control rats was seen. When administered in minipumps, ovine PRL (oPRL) and bovine GH (bGH) as well as a combination of oPRL and bGH led to an induction of estrogen receptors in Hx rat livers when dexamethasone treatment was given simultaneously. However, oPRL, bGH, and oPRL plus bGH failed to give a complete restoration of hepatic estrogen receptor levels. It is concluded that the estrogen receptor in rat liver is under multihormonal control and that glucocorticoids in combination with a pituitary factor(s) with similar properties to hGH seem to be responsible for the maintenance of the normal level of the receptor in female rats. Possibly, both GH and PRL are involved in the control of the receptor.
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