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1. |
Species and Strain Differences in Urinary Protein Excretion |
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Kidney and Blood Pressure Research,
Volume 8,
Issue 6,
1985,
Page 301-309
J.M. Alt,
B. Maess,
H. Hackbarth,
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摘要:
The physiological excretion of urinary protein is subject to great variation influenced not only by environmental and hormonal factors but also by genetics. The present study demonstrates that there is not only variation in respect to the excretion of plasma proteins but also of other types of proteins which are specific urinary proteins. There is a close relation between body weight and total protein excretion. However, male rats and mice do not fit the allometric line calculated for the other species studied. This is of special importance since these two species are often used in kidney research. The reason for this divergence in total protein is the excretion of sex-dependent low molecular weight proteins. The excretion of albumin, which is a marker of glomerular permeability and tubular reabsorption as well, shows a marked genetic variation between different rat strains. The data presented in this study demonstrate the general admissibility of transferring data from one species to the other but also the limitations in respect especially to the sex-dependent proteins which are excreted by some species.
ISSN:1420-4096
DOI:10.1159/000173062
出版商:S. Karger AG
年代:1985
数据来源: Karger
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2. |
On the Mechanism of Renal Vasoconstriction Induced by Acetylcholine in Indomethacin-Treated Dogs |
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Kidney and Blood Pressure Research,
Volume 8,
Issue 6,
1985,
Page 310-320
Sai-Sun Ho,
John C.H. Yun,
John R. Gill, Jr.,
Gerald D. Kelly,
Harry R. Keiser,
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摘要:
Renal arterial infusion of acetylcholine (ACh) in control dogs produced a natriuresis and diuresis and an increase in renal plasma flow (RPF) without a change in glomerular filtration rate (GFR) or in renin secretory rate (RSR). In dogs pretreated with indomethacin (Indo), an inhibitor of prostaglandin synthetase, renal arterial infusion of ACh first produced a rise, then a decline in urine flow, sodium excretion (UNaV) and GFR that was accompanied by a progressive fall in RPF and a progressive rise in RSR. The rise in RSR was potentiated by renal arterial infusion of an alpha-adrenergic receptor blocker, phenoxybenzamine (Phenoxy), and attenuated, but not completely abolished, by beta-adrenergic receptor blockade with propranolol (Prop). Chemical denervation with reserpine alone, or in combination with chronic surgical renal denervation, failed to prevent the fall in RPF, GFR and UNaV and the rise in RSR produced by ACh in Indo-treated dogs. Renal arterial infusion of Phenoxy and intravenous infusion of Prop, alone or in combination with renal arterial infusion of an angiotensin II antagonist, saralasin, failed to maintain the vasodilatory, diuretic and natriuretic effects of ACh in Indo-treated dogs. Elimination of endogenous vasopressin by hypophysectomy also failed to prevent the vasoconstriction induced by ACh in Indo-treated dogs. The results suggest that ACh produced renal vasoconstriction in Indo-treated dogs by mechanism(s) other than an increase in renal adrenergetic activity or an increase in the activity of the renin-angiotensin system. The results also suggest that the vasoconstriction was independent of vasopresin.
ISSN:1420-4096
DOI:10.1159/000173063
出版商:S. Karger AG
年代:1985
数据来源: Karger
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3. |
Properties of an Ecto-5’-Nucleotidase of the Renal Brush Border |
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Kidney and Blood Pressure Research,
Volume 8,
Issue 6,
1985,
Page 321-327
Michel Le Hir,
Stefan Angielski,
Ulrich C. Dubach,
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摘要:
A decrease of glomerular filtration rate can be observed during accelerated catabolism of ATP in kidney. It has been proposed that this effect is due to the increase in the renal production of adenosine from ATP. The last reaction in the pathway concerned is the conversion of 5’-AMP to adenosine. We found that brush border membranes purified from homogenates of the rat renal cortex carry out this reaction. The enzyme involved in the hydrolysis has the characteristic properties of ecto-5’-nucleotidases: It is inhibited by ATP, ADP, and by α, β-methyleneadenosine-5’-diphosphate, and it is not stimulated by magnesium. All catalytic sites are accessible from the outside of the vesicles. The Km of the enzyme for 5’-AMP is 5.77 µM. The enrichment of the 5’-AMP-hydrolyzing activity in the brush border fraction as compared to the homogenate is 9.2 ± 1.5 times. Histochemical staining of kidney sections reveals hydrolysis of 5’-AMP only at the brush border of the proximal tubule. We conclude that the brush border of the proximal tubule of the rat kidney possesses an ecto-5’-nucleotidase which has the same properties as the ecto-5’-nucleotidas
ISSN:1420-4096
DOI:10.1159/000173064
出版商:S. Karger AG
年代:1985
数据来源: Karger
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4. |
Long-Term Recovery of Superficial and Deep Glomeruli after Acute Renal Failure Evoked by Warm Ischemia |
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Kidney and Blood Pressure Research,
Volume 8,
Issue 6,
1985,
Page 328-337
Ö. Källskog,
I. Hellström,
K. Rissler,
M. Wolgast,
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摘要:
A study was made on the number of glomeruli in the outer cortex, midcortex, and inner cortex 4 weeks after 45min of warm ischemia, using alcian blue to stain functioning glomeruli. During this time the stainable glomeruli in the kidney as a whole had decreased in number from 32,000 to 16,800. The superficial glomeruli were reduced by only about 30%, whereas in the juxtamedullary zones the number of functioning nephrons were reduced by 80%. This shows that the juxtamedullary nephrons are the most susceptible to degeneration in the recovery phase of acute renal failure caused by ischemia. The decrease in the number of glomeruli was accompanied by a reduction in total glomerular filtration rate to about the same extent. In contrast, the kidney weight was reduced by only about 20%, suggesting compensatory hypertrophy of the remaining tubules. Fluid reabsorption, urine osmolality, and potassium-secreting ability also remained decreased. The contralateral kidney responded with a compensatory hypertrophy and an increase in glomerular filtration rate, whereas the number of glomeruli in the cortex as a whole and in the individual cortical zones in this kidney remained the same as in control kidneys. It is suggested that the trapping of red cells in the juxtamedullary circulation seen soon after restoration of circulation to kidneys subjected to warm ischemia will also cause a further degeneration of the juxtamedullary nephrons.
ISSN:1420-4096
DOI:10.1159/000173065
出版商:S. Karger AG
年代:1985
数据来源: Karger
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5. |
Impaired Sodium Excretion in Experimental Glomerulonephritis: an Explanation for the Controversies in the Literature |
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Kidney and Blood Pressure Research,
Volume 8,
Issue 6,
1985,
Page 338-347
A. Chachati,
J.P. Godon,
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摘要:
Considerable discrepancies exist in the literature concerning Na excretion by the rat kidney in experimental antiglomerular basement membrane (GBM) glomerulonephritis (GN). Previous studies in our laboratories demonstrated a disturbance in Na excretion with an impaired absolute (UNa × V) and fractional (FENa) excretion of Na after saline loading. However, most of the other authors in the literature failed to observe similar findings. The present study was undertaken to elucidate some of these controversies: We showed that a difference in Na excretion between anesthetized GN and normal rats might not be detected after a volume expansion if the latter is small or slow (FENa in GN 2 ± 0.1%, in normals 2 ± 0.2%; not significant). Only a rapid and important volume expansion is sufficient to unmask such a difference between the two groups (FENa 3 ± 0.3 and 6 ± 1%, respectively, p < 0.001), and detect an impaired Na excretion in GN animals. The same amount of NaCl was nevertheless administered during slow and rapid volume expansion. Similarly, in GN conscious rats only after a saline load or repeated water loads did we observe a significantly smaller UNa × V compared to normals while no difference was present between the two groups after a single water load. In the literature, all the authors, that failed to demonstrate a disturbance in Na excretion in anti-GBM GN, administered slow and small isotonic saline loads to their rats. The hypothesis we formulate to explain these controversies is that the nonobserved disturbance in sodium excretion in most of these studies is probably secondary to insufficient natriuretic st
ISSN:1420-4096
DOI:10.1159/000173066
出版商:S. Karger AG
年代:1985
数据来源: Karger
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6. |
Isoenzymes of N-Acetyl-β-D-Glucosaminidase in Kidney Cortex and Urine of Normal and Nephritic Rats |
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Kidney and Blood Pressure Research,
Volume 8,
Issue 6,
1985,
Page 348-356
Hans-Jacob Haga,
Knut-Jan Andersen,
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摘要:
Induction of acute Heyman nephritis in rats gave a significant increase in the urinary excretion of protein (p < 0.001) and N-acetyl-β-D-glucosaminidase (NAG; p < O.01) 14 days after injection of antibody. The isoelectric points (IP) of NAG were studied by chromatofocusing of the urine, serum and various lysosomal populations purified from kidney cortex homogenates of normal and nephritic rats. The chromatofocusing profiles for serum NAG (IP = 5.8) were totally different from the patterns found in normal and nephritic urines. The acidic IPs of NAG in normal urine (IP = 5.0) were changed into slightly more basic values in nephritic urine (IP =5.15). Similar changes were also demonstrated in normal urine after acidification and prolonged incubation. The chromatofocusing profile obtained for NAG in the large, dense lysosomes was almost identical to the pattern observed in nephritic urine and demonstrated IPs for NAG in a slightly more basic pH area than observed for small and medium-sized lysosomes. The difference in IP in normal and nephritic urines may therefore be due to an increased autolytic degradation of NAG or excretion of the enzyme from different populations of lysosomes
ISSN:1420-4096
DOI:10.1159/000173067
出版商:S. Karger AG
年代:1985
数据来源: Karger
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7. |
Author Index, Vol. 8, 1985 |
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Kidney and Blood Pressure Research,
Volume 8,
Issue 6,
1985,
Page 357-357
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ISSN:1420-4096
DOI:10.1159/000173068
出版商:S. Karger AG
年代:1985
数据来源: Karger
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8. |
Subject Index, Vol. 8, 1985 |
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Kidney and Blood Pressure Research,
Volume 8,
Issue 6,
1985,
Page 358-359
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ISSN:1420-4096
DOI:10.1159/000173069
出版商:S. Karger AG
年代:1985
数据来源: Karger
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9. |
Contents, Vol. 8, 1985 |
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Kidney and Blood Pressure Research,
Volume 8,
Issue 6,
1985,
Page -
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ISSN:1420-4096
DOI:10.1159/000173061
出版商:S. Karger AG
年代:1985
数据来源: Karger
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