Sensitization by Œstradiol to the Production of Experimental Nephrocalcinosis

Abstract

EARLIER experiments showed that excessive oral administration of mono- or dibasic-phosphates produces nephrocalcinosis in the rat, and that these renal lesions are aggravated by mineralocorticoids, such as deoxycorticosterone^1–3. Recent experiments revealed that, under similar experimental conditions, the nephrocalcinosis produced by oral administration of acid sodium phosphate is not aggravated by methyltestosterone, progesterone, corticosterone, Δ¹-cortisol acetate, or Δ¹-cortisone acetate, but curiously, œstradiol proved to be even more effective in this respect than deoxycorticosterone. It has long been known that folliculoid or ‘œstrogenic’ hormones exert a pronounced effect on calcium metabolism in birds, presumably because in the avian species the production of calcified egg shells is closely related to the action of sex hormones. In mammals, on the other hand, folliculoids do not exert any comparably pronounced effect upon calcium metabolism, and, therefore, the production of intense nephrocalcinosis by œstradiol (when given in combination with phosphates) was made the subject of a special study.