In earlier studies of the action of cortisol on tubular sodium reabsorption, we have found that the hormone enhance sodium reabsorption along all parts of the nephrone except the proximal site of the distal tubule. Because the mechanism of the action had not been defined, the working hypothesis was presented that cortisol promote DNA-dependent RNA synthesis that yields an increased rate of protein synthesis. The newly synthesized proteins appear to be enzymes involved in the coupling of metabolism to sodium tran-sport. Thus, studies of cortisol action on sodium reabsorption at the proximal tubule and of its inhibition by actinomycin D were performed in Wister strain male rats using the modified technique of “distal blo-ckade”. By administering cortisol and actinomycin D with triamterene, chlorothiazide and ethacrynic acid dulring mannitol infusion with replacement of urinary losses, increments in sodium excretion were used to calculate sodium reabsorption in the proximal tubule (TNa). On the control experiments, TNa was 72.2±5.8 pEq/min(mean±s. e.) and on the cortisol administered group, TNa increased to 110.5±7.8 4aEq/min (P<0. 005). However, the enhancement by cortisol has been completely inhibited by actinomycin D as TNa was 75.4+4.8 μEq/min. It has been concluded that the mechanism of cortisol action is the enhanced m-RNA synthesis that yields an increased rate of protein synthesis.

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The regional blood flow of rabbit kidney in the conditions of hemorrhagic shock, hemorrhagic shock after performing denervation to kidney, and hypertention produced by noradrenalin were measuced by new experimental method developed in our laboratory using P³² labeled erythrocytes. The blood pressure of abdominal aorta was measured by an electric manometer and the blood flow of renal artery was measured by a square electric magnetic flow meter. Rediological activity of β-ray from P³² labeled erythrocytes in the renal cortex was recorded with a Geiger-Muller tube (0.8 cm in diameter, Endowindow type) which was set just on the renal surface. Both renal cortical blood flow volume (mt/min.) and renal medullary blood flow volume (ml/min.) were caliculated from the recorded radiological activity (cpm). Other three experiments ; 1) Measurement of absorbed number of β-ray from P32 labeled erythrocytes rabbit kidney. 2) Measurement of cortical blood flow velocity, and 3) Measurement of rabbit renal cortical and medullary volume. The following results were obtained.1) The renal blood flow volume was about 45 ml/min. in normal condition. In hemorrhagic shock (40 mmHg) that was markedly decreased at the lebel of 44% of normal average and in noradrenalin admi- nistration (180 mmHg) at the lebel of 60%. At denervation of renal nerve, 20% of the renal blood flow volume increased and 7% of renal blood flow volume was decreased at hemorrhagic shock (40 mmHg) after performing denervation to kidney.2) The renal cortical blood flow volume was about 40 ml /min. in normal condition. Marked decresed renal cortical blood flow volume at hemorrhagic shock and at noradrenalin administration were 20 ml/min, and 27m1/min. Cortical blood flow volume of denerved kidney was 54 ml/min. At hemorrhagic shock after denerva- tion it was 46 ml /min.3) The ratio of the renal blood flow volume and renal cortical blood flow volume was 1 : 0.9 in normal condition. At hemorrhagic shock and noradrenalin administration it was changed to 1 : 0.8 and 1: 0.64. In conditions of denerved kidney and hemorrhagic shock after performing denervation to kidney it was 1: 0.92 and 1 : 0. 9, respectively.

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Urinary immunoglobulines have been found to consist of IgA, 7 S IgG, and subunit or fragment of immunoglobulines in the form of L-chains, Fc and Fc' fragment. It is generally accepted that 19 S IgM is not detected in normal urine, but IgM-related substance in low molecular form is present in urine collected after strenuous exercise. The purpose of this study is to investigate for the nature of three immunoglobulines in normal urine. Three immunoglobulines and its fragments were prepared from human serum and antisera were prepared in rabbits. Urine samples were collected from healthy male and concentrated approximately 1000 times. Fractio nation on Sephadex G-200 column chromatography of concentrated urine showed 3 peaks of FI, FII, and FIII. Urinary IgA, found in FI of normal urine, was shown to be identical antigenically with colostral IgA by Ouchterlony analysis with anti secretory IgA antiserum. Analytical ultracentrifugation of urinary IgA showed the sedimentation coefficient of 10.95 S. Native 7S IgG was detected in F 1I of normal urine, by Ouchterlony analysis with anti IgG antise-rum. L-chains and Fc and Fc' fragment were also detected in FIII of normal urine by immunoelectro-phoretic examination. Using anti Fd antiserum, H-chain and Fab fragment were not found in normal urine. IgM-related substance in normal urine was also examined in this report. By Ouchterlony analysis with anti IgM antibody in FIII of normal urine, IgM-related substance that had a deficient antigenic structure with that of reduced and alkilated IgM was detected. The sucrose density ultracentrifugation of FIII revealed that urinary IgM had sedimentation properties lower than 7S molecules.

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One handred and eighteen patients with mesangial proliferative glomerulonephritis were studied with renal clearances and renal biopsy. Follow-up studies were done on an average of 36 months (9 to 85). Nineteen patients died during the follow-up period. For histologic evaluation, each glomerulus was graded according to the degrees of mesangial prolifera-tion from 0 (almost normal) to N (hyalinized). Percentages of the observed glomeruli in each specimen were plotted against the degrees of glomerular lesions, thus glomerular lesion curves (GLC) were obtained. Tubulo-interstitial lesions were evaluated in a similar way to obtain tubulo-interstitial lesion curves (TILL). Patterns of GLC were classified into 4 groups : Group A (mainly grade I lesion) 52; Group B (mainly grade II) 17; Group B' (mainly grade II with few hyalinized glomeruli) 22; and Group C (more than half were hyalinized) 24 cases. Those with a mainly grade III lesion were rare (3 Cases) and were excluded from the following studies. TILC were also classified into 4 groups : Group a (almost normal) 50; Group a' (rather diffuse interstitial fibrosis without tubular atrophy) 32; Group b (focal fibrosis with tubular atrophy) 32; and Group c (advanced change with hypertrophic tubules) 19 cases. Clinical healing was observed in 12 of 115 cases. The initial histologic features of the healed cases were mainly Aa, and there was no way to differentiate the healing cases from the others. Renal clearances remained within the normal range in most of those with mild lesions, while those with advanced lesions tended to show a deterioration of renal function. Histologic evolution was examined in 37 cases. In most of Group A, the glomerular lesions were stationary, whereas Group B appeared to be more progressive except for one case which regressed to Group A. Progression to Group C was observed in 2 cases ; one from Group A and one from Group B'. Except for an unstable lesion of Group a', tubulo-interstital lesions progressed slowly from Group a to b to c.

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