THE ROLE OF THE ADRENALS IN THE PRODUCTION OF NEPHROSCLEROSIS BY ANTERIOR PITUITARY PREPARATIONS

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Abstract
IT HAS been shown that the synthetic adrenal compound desoxycorticosterone acetate (DCA) produces pronounced renal and cardiovascular lesions in a variety of animal species (Selye and Hall, 1943; Selye, Hall and Rowley, 1943; Selye and Hall, 1944; Selye and Pentz, 1943). Sensitivity to such treatment is increased if the animals are unilaterally nephrectomized and kept on a high sodium chloride intake. The lesions consist of nephrosclerosis, periarteritis nodosa and nodules in the heart resembling Aschoff bodies. The development of these lesions is inhibited by acidifying salts such as ammonium chloride (Selye, Hall and Rowley, 1945). Later it was found that unilaterally nephrectomized, sodium chloride treated rats develop these same lesions when exposed to various types of non-specific damage—especially cold—which induce adrenal cortical enlargement. This was interpreted as being due to the liberation of desoxycorticosterone-like compounds from the adrenal cortices through stimulation by endogenous hypophyseal corticotropic hormone.