ISSN:1420-4096    

DOI:10.1159/000172909

出版商:S. Karger AG    

年代:1983

数据来源: Karger

摘要:

Quantitative studies of endogenous lysozyme (low molecular weight protein) were performed in rats. Urine and plasma concentrations of lysozyme and inulin were measured spectrophotometrically. An improved lysozyme assay (standard curve established by using egg white-lysozyme) enabled us to determine the mean plasma concentration of endogenous lysozyme (4.4 µg· ml-1) and the urinary concentrations of endogenous lysozyme (between 0.1 and 3.8 µg · ml-1. The urinary concentrations of endogenous lysozyme were found to be dependent on urinary flow rate. High urinary concentrations (ULy) were found at low urinary flow rates (V). The excreted amount of endogenous lysozyme (ULy·V) was independent of urinary flow rate and yielded a constant value of 0.02µg·min-I. Mean glomerular filtration rate (GFR) was 1.2 ml- min-1 while clearance of endogenous lysozyme averaged 0.0039 ml · min-1. Inhibition of endogenous lysozyme reabsorption by cytochrome c was used to estimate the glomerular sieving coefficient of endogenous lysozyme in clearance experiments. CLy/GFR increased from a mean value of 0.0053 in control rats to 0.8 at maximal inhibition of tubular reabsorption of endogenous lysozyme by cytochrome c. Knowing the glomerular sieving coefficient, GFR and the lysozyme concentrations in plasma and urine samples, the filtered, excreted and reabsorbed lysozyme amounts could be calculated: 0.5% excreted and 99.5% reabsorbed. Reabsorbed endogenous lysozyme is stored in the kidney in high amounts (1,983 µg · g-1

ISSN:1420-4096    

DOI:10.1159/000172910

出版商:S. Karger AG    

年代:1983

数据来源: Karger

摘要:

Sprague-Dawley rats developed severe proteinuria 24 h after an intravenous injection with rabbit anti-rat kidney serum. Accumulation of polymorphonuclear leukocytes in the capillary lumen and their attachment to the glomerular basement membrane (GBM) were observed. The isolated and purified GBM of normal and nephritis-induced rats were observed by electron microscopy after negative staining. Although the GBM of normal rats appeared as a molecular sieve with uniform pores, the GBM of rats with nephritis had enlarged and elongated pores. An increase in the radius of glomerular pores may be responsible for the proteinuria.

ISSN:1420-4096    

DOI:10.1159/000172911

出版商:S. Karger AG    

年代:1983

数据来源: Karger

摘要:

Despite the absence of vasopressin, Brattleboro homozygous (DI) rats can concentrate their urine to hypertonic levels when deprived of drinking water. When DI rats are infused with vasopressin, freeze-fracture electron microscopy has revealed increases in intramembranous particle clusters (IPC) in papillary collecting duct luminal membrane that parallel the rise in urine osmolality. In the present study, we examined whether the increase in concentrating ability of DI rats dehydrated for 24 h was associated with a change in IPC. For comparison, oral water loading and 24-hour dehydration were used to suppress and stimulate endogenous vasopressin secretion in Long-Evans (LE) rats, and the effects on urine osmolality and IPC were examined. In LE rats, the induced changes in water balance resulted in alterations in IPC frequency that paralleled urine osmolality, whereas, in DI rats, frequency of IPC remained low under all conditions, even when urine osmolality rose to almost 1,000 mosm/kg H2O as a result of 24-hour dehydration. These results suggest that the increased concentrating ability of dehydrated DI does not depend upon increased water permeability of the papillary collecting ducts.

ISSN:1420-4096    

DOI:10.1159/000172912

出版商:S. Karger AG    

年代:1983

数据来源: Karger

摘要:

The mechanism of captopril-induced alterations in arterial pressure (AP), glomerular filtration rate (GFR), renal blood flow (RBF), and renal vascular resistance (RVR) was studied in pentobarbital anesthetized sodium-restricted dogs. In 7 dogs, captopril caused decreases in AP (16 ± 3%) and RVR (46 ± 5%), as well as increases in RBF (62 ± 12%) and sodium excretion (399 ± 73%). These responses were reversed by angiotensin II infusion at a rate sufficient to restore RBF to control levels. The captopril-induced increase in GFR (29 ± 8%) was partially reversed by the intravenous angiotensin II infusion to a level not significantly different from control. In 5 dogs, indomethacin increased AP (10 ± 2%) and RVR (38 + 8%); the slight decreases in RBF and GFR were not statistically significant. Subsequent captopril treatment decreased AP (20 ± 3%) and RVR (42 ± 4%), while RBF and GFR increased by 45 ± 8% and 32 ± 10%, respectively. These observations suggest that the renal response to captopril in sodium-restricted dogs is not dependent upon alterations in prostaglandin synthesis but, instead, is primarily due to diminished angiotensin II

ISSN:1420-4096    

DOI:10.1159/000172913

出版商:S. Karger AG    

年代:1983

数据来源: Karger

摘要:

Kallikrein activity in urine and in the renal cortex of the isolated rat kidney, perfused at constant pressure, decreased, while renal perfusate flow, glomerular filtration rate, excretion of sodium and of potassium and urine flow remained unchanged. Abrupt changes in perfusion pressure resulted in corresponding changes in renal perfusate flow, glomerular filtration rate, excretion of sodium and of potassium and urine flow. Urinary kallikrein increased little and transiently only, each time perfusion pressure was elevated. At the end of the experiments, a marked decrease in kallikrein activity in the renal tissue was found. From these results, it might be concluded that the excretion of kallikrein from the isolated perfused rat kidney resulted in a marked depletion of kallikrein stores in the kidney, probably due to an insufficient kallikrein synthesis.

ISSN:1420-4096    

DOI:10.1159/000172914

出版商:S. Karger AG    

年代:1983

数据来源: Karger

摘要:

The effects of a natriuretic factor contained in extracts of the atrial myocardium on an isolated renal Na+, K+-ATPase enzyme system were evaluated. Ultrafiltrates (molecular weight < 30,000) of boiled extract of rat atria and ventricles were prepared. Infusion of 100 µl of the atrial ultrafiltrate into bioassay rats resulted in a prompt, short-lived natriuresis and diuresis. However, addition of 100 µl of the atrial ultrafiltrate to 900 µl of a suspension containing Na+, K+-ATPase had no significant effect on enzymatic activity. Similarly, ultrafiltrates of ventricular extract also had no significant effect on Na+, K+-ATPase activity. These results indicate that the atrial natriuretic factor does not alter renal tubular sodium reabsorption by directly inhibiting the Na+, K+-ATPase enzyme syst

ISSN:1420-4096    

DOI:10.1159/000172915

出版商:S. Karger AG    

年代:1983

数据来源: Karger

ISSN:1420-4096    

DOI:10.1159/000172916

出版商:S. Karger AG    

年代:1983

数据来源: Karger

ISSN:1420-4096    

DOI:10.1159/000172917

出版商:S. Karger AG    

年代:1983

数据来源: Karger

ISSN:1420-4096    

DOI:10.1159/000172908

出版商:S. Karger AG    

年代:1983

数据来源: Karger