Effect of Desoxycorticosterone upon the Toxic Actions of Somatotrophic Hormone

Abstract

Summary and Conclusions

1. Experiments on rats—sensitized to mineralo-corticoid actions by unilateral nephrectomy and a high sodium intake—showed that somatotrophic hormone (STH) shares with desoxycorticoster-one acetate (DCA) the ability to produce: cardiac hypertrophy with histologic signs of a rheumatic-like myocarditis, hypertension, renal enlargement with microscopic evidence of malignant nephrosclerosis and an increased water turnover with proteinuria. 2. All these actions are greatly increased when STH and DCA are administered simultaneously, except for the rise in blood-pressure. The failure to develop hypertension under the influence of the two preparations may well be due to the fact that this hormone combination is extremely toxic and causes pronounced edema with obvious deterioration in the physical state of the animals. 3. It is concluded that STH sensitizes the tissues to the production of “collagen-disease-like” lesions by DCA. 4. STH also causes adrenocortical enlargement and prevents the compensatory atrophy of the adrenal cortex normally elicited by DCA. This effect may be due: to a contamination of our preparation with ACTH, to the compensatory secretion of ACTH by the pituitary of the STH-treated animal, or to a true corticotrophic action of STH. 5. Although earlier experiments had shown that even electrophoretically pure STH causes similar adrenal stmulation, we have no evidence either for or against the view that STH induces the adrenal cortex to produce miner-alo-corticoids. The “umineralo-corticoid-like” actions of STH could result solely from the sensitization of the peripheral tissues by STH. Increased mineralo-corticoid production by the adrenal cortex under the influence of STH may be an additional factor, but its possible participation remains to be demonstrated.