Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0155339 (Brown)
 12,436 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Brown Norway kininogen-deficient rats had very low levels of plasma kininogens and lower levels of plasma prekallikrein, compared with those of normal rats of the same strain. Systolic blood pressure, determined by the tail-cuff method, of 5-week-old kininogen-deficient rats (106 +/- 0.4 mm Hg, n = 7) and the rate of systolic blood pressure increase with age were not different from those in normal rats. Weekly injections of deoxycorticosterone acetate (5 mg/kg s.c.) with 1% sodium chloride solution in drinking water after uninephrectomy at 7 weeks of age caused a gradual increase in the blood pressure of normal rats, reaching a plateau at 18 weeks of age, whereas that of deficient rats rose rapidly to 158 +/- 6 mm Hg 2 weeks after the start of treatment and continued to increase slightly, becoming significantly higher than normal rats at 8, 9, 10, 11, and 12 weeks of age (p less than 0.05 or 0.01). The levels of urinary prokallikrein and active kallikrein were slightly higher in deficient rats before deoxycorticosterone acetate-salt treatment but were not significantly increased after this treatment, whereas these levels in normal rats were increased 3.6- and 4.7-fold by this treatment. Urinary free kinin, collected from the ureter in untreated deficient rats, was below the detection limit. The plasma level of low molecular weight kininogen, the substrate of glandular kallikrein, was decreased in normal rats during the treatment. Continuous subcutaneous injection of aprotinin by an osmotic pump to normal rats induced significant increase in blood pressure. These results indicate that glandular kallikrein may play a suppressive role in deoxycorticosterone acetate-salt hypertension.
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PMID:Suppression of rat deoxycorticosterone-salt hypertension by kallikrein-kinin system. 171 Jun 5

The Katholiek substrain of Brown Norway (BN/Kat) rats exhibits a very low level of circulating high-molecular-mass (HMW) kininogen and a partial deficiency in plasma prekallikrein. Northern blot analysis of liver RNA revealed that HMW kininogen and prekallikrein mRNAs are present in these rats with a similar size and abundance compared to control Brown Norway (BN/Orl) rats. The low-molecular-mass kininogen mRNA, encoded by the same kininogen gene as HMW kininogen mRNA by alternative splicing, is detected in both strains by dideoxynucleotide limited primer extension analysis. Measurement of HMW kininogen by radioimmunoassay was performed in liver subcellular fractions. It reveals that, in contrast to its absence in the cytosolic fraction, HMW kininogen in deficients rats is slightly more abundant in the microsomal fraction, than in control rats. These observations exclude both an abnormality at the level of gene transcription and a major structural modification of the transcribed RNA and of the synthesized HMW kininogen. They favour the hypothesis of an abnormal intracellular transport of the HMW kininogen in deficient rats.
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PMID:The high-molecular-mass kininogen deficient rat expresses all kininogen mRNA species, but does not export the high-molecular-mass kininogen synthesized. 318 25

To study the participation of the Hageman factor-related contact system of plasma in the pathogenesis of glomerulonephritis (GN), an anti-BM GN was induced in a group of 10 normal Brown Norway rats and another of seven Brown Norway BN/Mai Pfd f rats. The latter strain is characterized by a congenital deficiency of plasma prekallikrein and of high-molecular weight kininogen, with lengthening of the activated partial thromboplastin time. In the deficient group, one animal developed crescents in less than 25% of glomeruli, five in 25-50% and one in 50-75%. In the group of normal rats, extracapillary proliferation was of greater severity: one animal showed crescents in less than 25% of glomeruli, two in 50-75% and five in more than 75% of glomeruli. Although in both groups intense glomerular fibrin deposition was documented, the intensity of these deposits was less severe in the deficient animals. These data suggest, in the first place, that functional integrity of the contact system is not a necessary requirement for glomerular fibrinogenesis, other mechanisms being implicated in this phenomenon. On the other hand, this functional deficit has exerted a protective effect on crescent formation, which suggests that the contact system can play a role as a mediator of injury in glomerulonephritis, perhaps through the release of contact system-dependent mediators of inflammation.
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PMID:Role of the plasma contact system in the pathogenesis of experimental anti-GBM glomerulonephritis. 339 22

We studied the hypotensive effect of three carrageenans and of dextran sulphate in Brown Norway (BN) rats. The plasma of these BN rats is devoid of high molecular weight kininogen and poor in plasma prekallikrein. The hypotensive effect in BN rats was greatly reduced in comparison with the effects in normal rats. It was proportional to the thrombocytopenia induced by the sulphated polysaccharides and absent in rats made thrombopenic by antiplatelet serum. The hypotensive effect in BN rats was reduced by bromophenacyl bromide, mepacrine, aspirin, methysergide, promethazine and CCI 17810, and was unchanged after the administration of cobra venom factor, heparin, amino caproic acid, chloroquine, dexamethazone, lidocaine, propranolol, indomethacin, phenidone, imidazol, adenosine and cyproheptadine. The thrombopenic effect was reduced by methysergide and CCI 17810 and was not modified by bromophenacyl bromide and chloroquine.
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PMID:[Platelet stimulation and hypotensive action of carrageenans in the rat]. 667 65