実験的高血圧症に於ける副腎皮質機能の研究(第3報) : 副腎皮質の組織学的並びに組織化学的検索を中心にして : 第5編 実験的食塩高血圧症

Abstract

The author performed the histologic and histochemical study of the adrenal cortex, determination of 17-ketosteroids in urine to investigate the relationship between experimental salt hypertension and adrenal cortex.Male rats divided into three groups were given NaCl by mouth and/or by injection for about 6-9 months, group 1, 1-1.5 % NaCl solution was given by mouth, the total NaCl being 200-300 mg per day, group 2 was divided into two subgroups : (a) 1-1.5 % NaCl solution by mouth and intraperitoneal injection of 2 % NaCl solution, the total NaCl being 200-300 mg per day, (b) intraperitoneal injection of 2 % NaCl solution, the total NaCl being 200-300 mg per day. For the first 72 days no differences were observed between subgroups (a) and (b). Since then 300-400 mg of NaCl daily has been given orally to both subgroups. Group 3, which was control, received 50 mg of NaCl per day. After 5 months NaCl-loading was withdrawn in some rats.In the course of experiments, the author performed the clinical examinations including the measurement of blood pressure, fluid intake, urinary volume, urinalysis, body weight, Cl in urine, and urinary 17-ketosteroids excretion. After the animals were sacrificed, the author performed the histologic and histochemical examination of the adrenal cortex.The summary and conclusion of this study are as follows : 1) The NaCl-loading could produce a marked hypertension which sustained at the level of about 200 mm Hg. The elevation of blood pressure at that time was proportional to the amount of loaded salt.2) Adrenal cortical changes occured in experimental salt hypertensive rats were a progressive disuse atrophy of zona glomerulosa in proportion to the amount of loaded salt, and they were reversible.On the contrary, there appeared an enlargement of zona fasciculatea, namely the sign of stress in this zona. The changes in zona fasciculata was almost proportionately to the amount of urinary 17-ketosteroids excretion, but no relation was found between 17-ketosteroids excretion and elevation of blood pressure.From the changes of zona glomerulosa, it is assumed that the adrenal cortex would not secrete mineralocorticoids in salt hypertension, and that zona glomerulosa would not be concerned with salt hypertension. The direct causative factor in salt hypertension would be the excessive retention of sudium.