Abstract

The relative specific activity of the inorganic phosphorus of the adrenal gland of rats 2 hours after an intraperitoneal injection of inorganic P32 was increased by the administration of adrenaline, histamine, or commercial pitressin. These substances are all known to cause a depletion of the adrenal ascorbic acid. The effect on the adrenal phosphorus metabolism, like the effect on the adrenal ascorbic acid, was absent or greatly reduced in hypophysectomized rats and in rats previously treated with cortisone.In hypophysectomized rats the administration of exogenous ACTH caused an increase in the relative specific activity of the adrenal inorganic P and, again like the adrenal ascorbic acid depletion, this increase was not abolished by previous treatment with cortisone.These results, together with other observations on adrenal phosphorus metabolism previously reported for rats exposed to a cold environment, strongly suggest that the incorporation of inorganic P32 into the adrenal gland is controlled by the same factors that control the depletion of adrenal ascorbic acid. It is, therefore, concluded that the incorporation of inorganic P32 into the adrenal gland is a valid index of the activity of the adrenal cortex.

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