We studied on the reaction of renin and angiotensinogen in vitro, using hog plasma, semipurified hog renin substrate etc. In the first, plasma and renin substrate solution were incubated at pH 5.5 and 37C with a constant amount of renin, EDTA and DFP, respectively. The angiotensin preduced was distinctly less in the plasma than in the substrate solution at any time course of incubation. Suchh a difference on the angiotensin formation was not due to a disagreement of angiotensinase activity between the two incubation mixtures, and of course not angiotensinogen concentration. In our experimentall conditions, heparin had little effect on renin activity. Furthermore, we employed the Lineweaver-Burk plot technique to make clear kinetically the difference of the reactivity between the two mixtures. It seemed to us that the results indicated the existence of a competitive inhibitor to renin-angiotensinogen reaction in plasma.

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Changes in structure and function of rat kidney have been observed from birth to the mature stage. The concentration gradient of urea and total osmoactive solutes from cortex to papilla is not observed immediately after birth in rat kidney, but substantial cortico-medullary gradient is found one monthh after birth ([Papilla/Cortex] total osmotic pressure ratio : 1. 8, [Papilla/Cortex] urea ratio : 4.6). Marked heterogeneity of nephron popullation is seen. In general, nephron development of outer cortex is poor, whereas that of inner cortex is much fetter after birth. There is no difference in structure between nephrons of outer cortex and inner cortex in adult rat by means of microdissection. From the above-mentioned fact, it is thought that immature nephron cannot work as adult as for kidney particularly due to insufficient counter-current mechanism after birth and, one month after birth, , nephron can act as well as adult kidney.

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This study was undertaken to investigate the clinical significance of hyperuricemia associated with essential hypertension, and to elucidate the role of the kidney in the pathogenesis of this hyperuricemia. 1) Sixty-six subjects of 189 hypertensives whose glomerular filtration rate was normal and in whom treatment with thiazides was discontinued at least for two weeks prior to the study, showed hyperuricemia (above 7.0 mg per 100m1). 2) The incidence of hyperuricemia was not directly related to the level of blood pressure, but the incidence among the subjects with hypertensive vascular complications was higher than among those without them. Although the further study must be required to elucidate the direct role of hyperuricemia in the development of the vascular complications, hyperuricemia seems likely to be one of poor risk factors in the process of essential hypertension 3) The clearance study elucidated that urate clearance was specifically diminished in essential hypertesion, while the calculated filtered load of urate in essential hypertension was larger than in the normals. 4) Tracer studies with glycine-14C and/or uric acid-'4C demonstrated that de novo synthesis of uric acid in hypertension was almost normal, although the uric acid pool in hypertension was comparable with that of gout. 5) The hypertonic saline infusion and ammonium chloride loading studies revealed the presence of a competitive transport mechanism between urate and the other (organic) acids in the renal tubules. Hyperuricemia associated with essential hypertension might result from disturbance (s) of this tubular competition. 6) These observations may account for the mechanism of hyperuricemia associated with essential hypertensin, however, it remains to be elucidated why hyperuricemia develops in only about one-third of essential hypertensive subjects.

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Clinico-histopathological study inclusing steroid effects on primary nephrotic syndrome of 56 cases was performed and carried out the following results. Each cases were examined with electron microscopy and Lounted the mean values of the width of basement membrane of capillary loops.They were divided three groups according the width of basement membrane ; 1) less than 5000Å, 2) 5000-10000Å, 3) more than 10000Å. The thickening of basement membrane were closely related the clinical responsibility of steroid hormon. The first group, less than 5000Å was very effected with steroid treatment, but the third group, more than 10000Å was no responsed with the same therapy. The second group, 500010000Å, however, was showed no constant effect to steroid therapy. The third group consisted with all membranous glomerulonephritis electron microscopically. The first group, however, consisted with minimal change.

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