Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.21.7 (plasmin)
 9,023 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Masugi nephritis was induced in dogs in which platelet count, fibrinogen, antithrombin activity, plasma prekallikrein and immediate plasmin inhibitors were coincidentally decreased immediately after the injection of nephrotoxin serum. It was found that the grade of decrease of urinary kallikrein excretion following these immediate reactions were parallel with the grade of renal damages. By the pretreatment with heparin or the defibrination with snake venom, however, the histological findings of Masugi nephritis showed rather severe damage. Based on the consumption of coagulation factors, kallikrein, kinin and their inhibitors in the development of this nephritis, it was postulated that inauguration of coagulation and activation of kallikrein contributed to the development of glomerulonephritis. The treatment or prevention of this coagulation process with heparin or snake venom, however, gave untoward effects on the pathological process in this experiment.
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PMID:Participation of kallikrein, coagulation/fibrinolysis parameters in the development of glomerulonephritis. 49 36

Using a modified model of Masugi's nephritis of rats, various enzymatic activities in urine, serum and renal tissue (glomeruli or cortex) were determined at appropriate intervals after the administration of anti-kidney serum and compared with the urinary protein content and the kidney weight. In the urine, alkaline phosphatase (Al-Phosase), acid phosphatase (Ac-Phosase) and N-acetyl-beta-glucosaminidase (NA-beta-Gase) activities remarkably increased after the induction of nephritis, reached their peaks on the 10th day and reverted to almost the normal levels on the 30th day. The patterns of time course of these enzymatic activities were similar to patterns seen in the urinary protein content and the kidney weight. In the serum, the Al-Phosase activity decreased slightly, while NA-beta-Gase activity increased slightly. The Ac-Phosase activity in serum remained at normal levels during the experimental periods. In the glomeruli, the bound activities of these three enzymes decreased with nephritis, showing a negative correlation with results in the urine. On the other hand, fibrinolytic activities in the urine (plasmin-like enzyme) and renal cortex (plasminogen activator) also paralleled the urinary protein content and the kidney weight in the course of the disease. These results suggest that the Al-Phosase, Ac-Phosase and NA-beta-Gase excreted into urine in cases of nephritis may be mostly derived from damaged renal cells and one part of Al-Phosase may also come from the plasma. Moreover, the increase of plasmin-like enzyme in urine is considered to be due to the increase of plasminogen activator in the renal cortex. Thus, the determination of these enzymatic activities in the urine should be useful for evaluating effects of drugs for the treatment of nephritis.
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PMID:Pharmacological studies on experimental nephritic rats (9). Changes in activities of urinary enzymes in the modified type of Masugi's nephritis and their sources. 720 60