Formation of the glomerular basement membrane in developing human renal glomerulus is observed, and experimentally the metabolism of lamina densa in normal and nephrotic rats are investigated by means of electron microscopy. 1) In immature glomeruli, two components, that is, epithelial and mesangial take part in formation of the glomerular basement membrane, and the double-membrane structures are observed. 2) In normal rats, the basement membrane is maintained itself in constant thickness, as keeping balance of the formation of new fibrils and the destruction of old ones. The turn over of the base-ment membrane component is mainly taken place from the epithelial surface. 3) Glomerular basement membrane has extremely and variably thickened in nephrotic rats, and there are two ways of new formation of the basement membrane, the one from epithelial and the other mesangial side. Histological changes can be divided into following two types.1. Formation from epithelial side and destruction on endothelial side are increased in violence si-multaneously, and then the original lamina densa is replaced rapidly with new increment.2. Formation from both epithelial and mesangial side are enhanced, and the original lamina densa has its location just as sandwiched by new increment. 4) There could be found no any correlations between the fusion of foot processes and the formation of glomerular basement membranes, however, it is suggested that dense material in the epithelial cell may produce new lamina densa.

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To clarify cholesterol metabolism in experimental nephrosis, the cholesterol biosynthesis in the liver and kidney of nephrotic mice induced by aminonucleoside was studied. Male mice weighing abut 20 g were divided in to the following 3 groups of control group, aminonu-cleoside treated group and aminonucleoside plus aspartic acid salts treated group. The animals received daily subcutaneous injection of aminonucleoside at a rate of 1.5 mg per 100 g body weight. At the same time aspartic acid salts (50 : 50 mixture of K and Mg salts of 1-aspartic acid) were injected daily sub-cutaneously at a rate of 300 mg per kg body weight. Control mice received daily subcutaneous injection of 0.9% saline solution. On the seventh day of the experimental period, 5 μci of sodium acetate-1-¹⁴C or 0.12 μci of dl-me-valonic acid-2-¹⁴C per 20 g body weight were injected subcutaneously into each mice of each group respectively. One hour following initial isotope administration, all animals were sacrificed. Liver, kidney and blood sample were taken. The following result's were obtained.1. Aminonucleoside increased the incorporation of hepatic cholesterol from both acetate-1-¹⁴C and dl-mevalonic acid-2-¹⁴C. While the joint usage of aspartic acid salts inhibited the increased incorporation of cholesterol from mevalonic acid, that from acetate was not inhibited.2. Aminonucleoside increased the cholesterol biosynthesis from dl-mevalonic acid-2-¹⁴C in kidney, While the cholesterol biosynthesis from acetate-1-¹⁴C showed no changes. The joint usage of aspartic acid salts inhibited the increased incorporation of cholesterol from mevalonic acid and showed no changes on the cholesterol biosynthesis from acetate.3. The increased incorporation of acetate in to blood cholesterol induced by aminonucleoside was not inhibited by the joint usage of aspartic acid salts, while the increased incoporation of mevalonic acid in to blood cholesterol was inhibited by the joint usage of aspartic acid salts.4. The results outlined above indicate that aminonucleoside stimulates cholesterol biosynthesis by acting on some reaction between mevalonic acid and cholesterol, While the joint usage of aspartic acid salts inhibit an increased cholesterol biosynthesis induced by aminonucleoside by affecting somewhere bet-ween mevalonic acid and cholesterol.

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The examination of the decrease in salivary sodium-potassium ratio has been considered significant in the diagnosis of hyperaldosteronism. The degree of the change in the ratio, however, was uncertain, and the present investigation was done to examine the diagnostic significance of the ratio. The sodiumpotassium ratio was obtained by flame photometry with the mixed saliva collected at 8 in the morning by the method of chewing a small piece of paraffin block. 1. The salivary sodium-potassium ratio was 0.65 and below in 7 cases of primary aldosteronism, whereas that in the normal control was in the range of 0.60-2.50. However, low ratios of 0 50 and below and 1.00 and below were also observed in two cases of malignant hypertension and 4 cases of renovascular hypertension, respectively. In 12 cases of essential hypertension, the ratio was 0.70 and over. An increase of the ratio to 0.70 and over was observed in 5 postoperative cases of primary aldo-steronism two weeks after the removal of the adrenocortical adenoma. Since low salivary sodium-potassium ratio was also observed in secondary aldosteronism such as mali-gnant hypertension and renovascular hypertension, the decrease in the ratio can not be served as the criterion in the differential diagnosis of aldosteronism, though the ratio of 1.00 and over may suggest that the case is not possibly of primary aldosteronism. 2. The renal potassium clearance when loaded by sodium thiosulfate (Cx(Na₂S₂O₃)) is high in primary aldosteronism, and the clearance is known to be mainly affected by the mineralocorticoid activity. A negative correlation was observed between salivary sodium-potassium ratio and simultaneously obtai-ned Cx (Na₂S₂O₃) in total 35 cases of primary aldosteronism, malignant hypertension, renovascular hype. rtension, essential hypertension, and Addison's disease, as well as in the normal control. The salivary sodium-potassium ratio may have some relation to the mineralocorticoid activity. 3. The salivary sodium-potassium ratio in the normal case was high in the morning, low in the da-ytime, and became high at night ; the urinary excretion of sodium and potassium was high in the dayti-me and low at night. Similar rhythm of the salivary sodium-potassium ratio was observed in primary aldosteronism and Addison's disease, while the diurnal rhythm of urinary excretion in primary aldosteronism was opposite to that of the control, and that in Addison's disease was often uncertain. The diurnal variation in the salivary sodium-potassium ratio seems to be affected by certain factor(s) different from the adrenocortical function, and the ratio may be controlled by some mechanism different from that controlling the urinary excretion of sodium and potassium.

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In this study I have investigated the role of plasma renin activity in blood pressure regulation of pthe experimental renal hypertensive dog (Goldblatt' type). Removal r of the adrenals was followed, by lowering of blood pressure approximately 25%, and then plasma renin activity (by the method of Page et al) increased. In experimental renal hypertensive dogs subjected to complete adrenalectomy, it could be observed that arterial blood pressure did not increase in spite of the high renin concentration. Cortisone 100 mg/dog/day` administration to such animals for 7 days rose blood pressure over normal level, whilee plasma, renin activity was not different from that of the non-administered. In 2 dogs the accessory adrenals .were found, , high renin activity and hypertension were observed. It is apparent, therefore, that arterial blood pressure has no correlation to plasma renin concentration. Adrenalectomy reduced serum sodium content and increased potassium. But in 2 dogs with cortisone administration, these ions restored to normal levels. GFR and RPF were decreased approximately 20% with adrenalectomy and 50% with adrenalectomized Goldblatt' dog. These were not influenced with cortisone administration. The intravenous' injection of synthetic angiotensin-II (Hypertensin Ciba) 0, 5 γ into such animals did not produce a significant decrease of the pressor response. There were no correlation between pressor response and plasma renin activity or serum sodium content. Blood catecholamines were hot influenced significantly in all experimental stages. These results were discussed, it is suggested that increased plasma, a renin activity and secretion of aldosterone or glucocorticoids from the adrenal cortex may be an essential factors in the developement of the experimental renal hypertension.

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