Hormonal regulation of ascorbic acid in the adrenal of the rat.

Fifteen days after hypophysectomy of rats the concentrations of ascorbic acid (AA) in adrenals, liver, blood and urine are lower than in normal rats or in rats 1 day after hypophysectomy. Despite the low levels the percentage AA depletion after administration of ACTH and the subsequent repletion to the pre-ACTH level are normal. Lack of corticosteroids is not the cause of the low AA levels, as shown by experiments in 15 days adrenalectomized rats and in rats treated with low doses of dexamethasone. Fifteen days treatment with high doses of dexamethasone lowered the AA concentrations in adrenals, liver and blood. Treatment with long-acting ACTH maintained adrenal weight but not adrenal and blood AA. A high dose of ACTH lowered these levels. The administration of AA markedly increased the AA levels in blood, but did not normalize its concentration in the adrenals, not even when the size of the adrenals was maintained by treatment with long-acting ACTH. Growth hormone, in particular when administered together with long-acting ACTH, markedly raised the AA concentration in the adrenals but hardly affected the AA blood level. Rats with high blood levels of prolactin induced by pituitary grafts in the kidney also had clearly higher AA levels in adrenals, but not in blood. These results indicate that, although acute AA release from the adrenal is caused by ACTH, AA uptake to a certain concentration is not controlled by the pituitary gland, and above this concentration is promoted by growth hormone and prolactin. In the liver AA release may also be caused by ACTH but the AA production is promoted by other as yet unidentified pituitary factors.