Grötsch, Hropot, Klaus, Malerczyk and Mattenheimer: Enzymuria of the rat: Biorhythms and sex differences 343 Summary: Alanine aminopeptidase, -glutamyltransferase and N-acetyl-ß-Z)-glucosaminidase were measured daily over 65 days in 24-hour urine of male and female Wistar rats. The mathematical evaluation was based on the Föw/er-analysis. The excretion of alanine aminopeptidase and -glutamyltransferase was higher in male than in female rats. This sex-dependent difference was not observed for N-acetyl-ß-/)-glucosaminidase. The excretion of the 3 enzymes followed a biorhythm with a dominant period of 7 days forglutamyltransferase and N-acetyl-ß-£>-glucosaminidase and one of 9 days for alanine aminopeptidase. Biorhythms and sex differences of enzymuria should be considered in experimental designs. Enzymurie der Ratte: Biorhythmen und GeschlechtsdifferenzenZusammenfassung: Alaninaminopeptidase, -Glutamyltransferase und N-Acetyl-ß-D-glucosaminidase wurden täglich über 65 Tage bei männlichen und weiblichen Wistar-Ratten im 24 h-Urin gemessen. Die Ergebnisse wurden vermittels fbwr/er-Anälyse ausgewertet. Die Ausscheidung von Alaninaminopeptidase und -Glutamyltransferase zeigte deutliche geschlechtsabhängige Unterschiede, wobei von männlichen Ratten mehr ausgeschieden wurde als von weiblichen Tieren. N-Acetyl-ß-/)-glucosaminidase zeigt diese Unterschiede nicht. Die Ausscheidung der drei Enzyme unterlag Biorhythmen mit Periodenlängen von sieben Tagen für -Glutamyltransferase und N-Acetyl-ß-jp-glucosaminidase und neun Tagen für Alaninaminopeptidase. Biorhythmen und Geschlecht$differenzen in der Enzymurie sind bei Versuchsplanungen zu berücksichtigen. Introduction. , « , , years the rat has been used äs the main experimental Urine enzymes äre being used with increasing animal in enzyine excretion studies. This animal frequency äs sensitive indicatöfs for early detection shows significant enzymuria when substances are of renal damage. Many investigatiöns include a administered which cause increased enzymuria in discussipn of biörhythms in man and animals, re-man. The rat tolerates well single-cage housing in speetively (l -3), A few reports on experimental ani-long term experiments. Enzymes with the smallest mal models document this coherence of biörhythms experimental Variation and good reproducibility are and nephrptoxicity with a close correlation between alanine aminopeptidase, -glutamyltransferase and enzyme excretion and renal damage. Of the large N-acetyl-ß^jD-glucosaminidase. The aim of this study nuinber of urine enzymes, it is mainly those from the was to apply modern mathematical methods to the proximal tübular cells that are of particular interest investigation of biörhythms and sex-specific for toxicological and clinical investigatiöns. In recent differences in the excretion of these enzymes over a
Inhibition of the angiotensin converting enzyme (ACE) with ramipril was studied in male Wistar rats during long-term inhibition of nitric oxide (NO) synthase by NG-nitro-L-arginine methyl ester (L-NAME). Chronic treatment with L-NAME in a dose of 25 mg/kg per day over 6 weeks caused myocardial hypertrophy and a significant increase in systolic blood pressure (245 +/- 16 mmHg) as compared to controls (155 +/- 4 mmHg). Animals receiving simultaneously L-NAME and ramipril were protected against blood pressure increase and partially against myocardial hypertrophy. L-NAME caused a significant reduction in glomerular filtration rate (GFR: 2.56 +/- 0.73 ml.kg-1.min-1) and renal plasma flow (RPF: 6.93 +/- 1.70 ml.kg-1.min-1) as compared to control (GFR: 7.29 +/- 0.69, RPF: 21.36 +/- 2.33 ml.kg-1.min-1). Addition of ramipril prevented L-NAME-induced reduction in GFR and renal plasma flow. L-NAME produced an elevation in urinary protein excretion and serum creatinine and a decrease in potassium excretion which was antagonised by ramipril. L-NAME-induced increase in plasma renin activity (PRA) was further elevated with ramipril treatment. Isolated hearts from rats treated with L-NAME showed increased post-ischaemic reperfusion injuries. Compared to controls duration of ventricular fibrillation was increased and coronary flow reduced. During ischemia the cytosolic enzymes lactate dehydrogenase and creatine kinase, as well as lactate in the venous effluent were increased. Myocardial tissue values of glycogen, ATP, and creatine phosphate were decreased, whereas lactate was increased.(ABSTRACT TRUNCATED AT 250 WORDS)
An open study was carried out in ten healthy, male volunteers in order to investigate the renal tolerance of cefpirome (HR 810), a new cephalosporin antibiotic. Subjects received a single dose of 1.0 g of cefpirome and then repeated doses of 1.0 g of cefpirome twice daily for five days. Urine was collected in several fractions during the study and the urine excretion, excretions of creatinine, N-acetyl-beta-D-glucosaminidase, gamma glutamyltransferase, alanine aminopeptidase and lactate dehydrogenase were calculated in 12-hour fractions. Serum creatinine (using an enzymatic method), beta 2-microglobulin concentrations and creatinine clearance were also determined. Based on the findings of these renal enzymes, renal tolerance was good. This was also confirmed by creatinine clearance calculations and follow-up of serum beta 2-microglobulin levels. Cefpirome showed good renal tolerance without any signs of nephrotoxicity in this study with the methods used.
Aim of the present study was to investigate the influence of the angiotensin II (ANG II) subtype 1 (AT(1)) receptor blockers fonsartan and losartan on blood pressure, cardiac -dynamics and -metabolism as well as functional and morphological changes in the kidney of rats after long-term inhibition of the nitric oxide (NO) synthase by N(G)-nitro-L-arginine methyl ester (L-NAME). Oral chronic treatment with L-NAME in a dose of 25 mg/kg/d over 6 weeks caused a significant increase in systolic blood pressure (198+/-13 mmHg) when compared to untreated rats (144+/-4 mmHg). Animals receiving simultaneously L-NAME and fonsartan (10 mg/kg/d) or losartan (30 mg/kg/d) were protected against blood pressure increase. L-NAME treatment caused a significant decrease in glomerular filtration rate (GFR) from 4.52+/-0.81 to 1.34+/-0.26 ml/kg(-1)/min(-1) and renal plasma flow (RPF) from 10.52+/-1.29 ml/kg(-1)/min(-1) to 5.66+/-1.06 ml/kg(-1)/min(-1). Co-treatment with fonsartan and losartan prevented L-NAME-induced reduction in GFR and RPF. There was no difference in urine, sodium and potassium excretion in groups under investigation. Plasma renin activity (PRA) was further stimulated by fonsartan and losartan treatment. L-NAME produced a significant elevation in urinary protein excretion which was antagonised by both AT(1) blockers. Isolated hearts from animals treated with L-NAME showed a significant prolongation in the duration of ventricular fibrillation and a significant decrease in coronary flow as compared to control hearts. Treatment with fonsartan and losartan significantly decreased the duration of ventricular fibrillation as compared to L-NAME group. In addition, both AT(1) blockers given alone significantly reduced the duration of ventricular fibrillation as compared to hearts from untreated controls. During ischemia the cytosolic enzymes lactate dehydrogenase and creatine kinase as well as lactate in the coronary effluent were significantly increased in the L-NAME group. Myocardial tissue values of glycogen, ATP, and creatine phosphate were decreased, whereas lactate was increased. Fonsartan and losartan treatment totally abolished these effects. Histological examination of kidneys revealed that simultaneous administration of fonsartan and losartan with L-NAME abolished L-NAME-induced arteriolar hyalinosis, segmental sclerosis of glomerular capillaries and focal tubular atrophies. In conclusion, long-term blockade of ANG II subtype AT(1) receptors by fonsartan and losartan prevented L-NAME-induced hypertension, renal insufficiency, as well as cardio-dynamic, cardio-metabolic, and morphological deteriorations.
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