Fate of Vasopressin Perfused into Nephrons of Wistar and Brattleboro (Diabetes Insipidus) Rats

1980 ◽  
Vol 58 (2) ◽  
pp. 139-144 ◽  
Author(s):  
M. D. Lindheimer ◽  
A. Reinharz ◽  
A. Grandchamp ◽  
M. B. Vallotton

1. Iodinated vasopressin was microinjected into early proximal or distal tubules of Wistar and Brattleboro (diabetes insipidus) rats. Sites of infusion were determined by the lissamine green transit time method. 2. Urinary recovery of 125I after proximal and distal injections was 89 ± se 1·7% and 94 ± 1·0% in Wistar rats (corrected for inulin) and 81 ± 20 and 92 ± 2·0% in Brattleboro rats (uncorrected); injection of hormone into vascular stars resulted in similar 125I recoveries from punctured and contralateral kidneys. 3. Radioactive substances excreted after perfusing proximal and distal sites in Brattleboro animals, and 125I-labelled hormone added to urine from the contralateral kidney, bound similarly to a specific arginine vasopressin antiserum and demonstrated similar radioactive elution profiles after passage through Sephadex G25 columns. 4. Incubation of labelled and unlabelled vasopressin with rat kidney homogenates resulted in similar and complete degradation of the hormone. 5. Results indicate that most of the vasopressin injected into either proximal or distal nephrons enters the urine intact, and no evidence of tubular secretion was found when perfusing vascular stars. Enzymes in rat renal tissue degrade labelled vasopressin, but the ability of the proximal tubule to hydrolyse the 125I-labelled vasopressin is limited, especially when compared with that reported for several linear peptide hormones.

1985 ◽  
Vol 63 (12) ◽  
pp. 1581-1585 ◽  
Author(s):  
María M. Elías ◽  
Elbio J. Comin ◽  
Elena J. Ochoa ◽  
Emilio A. Rodríguez Garay

Previous studies in rats have suggested that the urinary excretion of unconjugated bilirubin (UB) comprises only a small fraction of the pigment that reaches the tubular lumen by glomerular filtration and escapes from tubular cell reabsorption. However, additional data also indicated that UB interacts with renal peritubular cell membranes impairing the secretion of p-aminohippurate (PAH). In this study we examined the possibility of a secretory step which could also be involved in the renal excretory mechanism for UB. An isolated rat kidney preparation was used, and the uptake of UB by renal tissue, the UB appearance in the urine, and the secretion of PAH were analyzed throughout the perfusion. The results indicated that the UB urinary excretion rate changed independently of UB filtered load. The latter remained almost unchanged during the perfusion, whereas the excretion rate of UB and the UB-to-creatinine (Cr) clearance ratio increased significantly. Furthermore, a relationship between the uptake of UB by the kidney, the UB-to-Cr clearance ratio, and the decrease in PAH secretion rate, was proved. In addition, when probenecid was added to the perfusate solution the cumulative uptake of UB by the kidney and the rate of excretion of UB in the urine were diminished. We conclude that the mechanism of UB excretion by the kidney may be considered as the result of a process involving glomerular filtration plus tubular secretion followed by a back diffusion step from the lumen in a similar way to other endogenous compounds, thus explaining the virtual absence of UB from the normal urine.


Medicina ◽  
2010 ◽  
Vol 46 (3) ◽  
pp. 204
Author(s):  
Marina Aunapuu ◽  
Andres Arend ◽  
Mai Ots ◽  
Mara Pilmane

Cell proliferation and apoptosis in the remnant rat kidney after treatment with lowdose irradiation was investigated. Material and methods. In the first group (n=9), adult male Wistar rats underwent 5/6 nephrectomy (NPX); in the second group (n=9), NPX was combined with low-dose irradiation. Rats without surgery and irradiation formed the control group (n=9). Results. Hypertension and proteinuria induced by NPX were decreased by 3-Gy irradiation. The 5/6 NPX rats showed a dramatic increase in proliferating and apoptotic cells in the glomeruli and in the distal tubules at week 2, which was significantly decreased by low-dose irradiation. Conclusion. The data demonstrate that low-dose irradiation is a factor slowing the process of chronic renal injury.


1989 ◽  
Vol 256 (1) ◽  
pp. F100-F106
Author(s):  
T. Bjerke ◽  
E. I. Christensen ◽  
N. Boye

Micropuncture studies were performed to assess the reabsorption and metabolism of the vasoactive peptide neurotensin (NT) in individual nephron segments and compare it to the handling of the closely related peptide bradykinin (BK). Rat proximal and distal convoluted tubules were microinfused with [3H]NT or [3H]BK. In a second set of experiments, [3H]NT and its metabolites in the ureteral urine were separated and characterized using high-performance liquid chromatography (HPLC) technique. The urinary recovery of 3H-labeled material was 31% when proximal tubules were microinfused with [3H]NT and 94% when distal tubules were infused. For proximal tubules the label recovered in the ureteral urine consisted exclusively of metabolites of NT and appeared as tyrosine, NT1-11, probably NT9-13, and two uncharacterized products. For distal tubules, 9% chromatographed as intact NT in the urine and except for the proportion the metabolites were almost identical to those found when proximal tubules were microinfused. Following microinfusion of [3H]BK into proximal tubules, the urinary recovery of 3H-labeled material was 19%. There was no correlation between fractional reabsorption of 3H-labeled material and proximal tubular length when [3H]NT or [3H]BK was microinfused. In vitro incubation studies with rat ureteral urine showed extensive degradation of NT yielding tyrosine, NT1-6, probably NT9-13, NT, and two uncharacterized products. In contrast, there was no detectable breakdown of BK over a 32-min period. Finally, [3H]NT was incubated in rat serum, and these experiments also showed degradation of the peptide but not to the extent as when incubated in ureteral urine.(ABSTRACT TRUNCATED AT 250 WORDS)


1986 ◽  
Vol 136 (3) ◽  
pp. 947-954 ◽  
Author(s):  
Shigeyuki Takeda ◽  
Eiji Kusano ◽  
Naoki Murayama ◽  
Yasushi Asano ◽  
Saichi Hosoda ◽  
...  

2020 ◽  
Vol 1 (1) ◽  
pp. 10-14
Author(s):  
Seyed Salam Kohnepoushi ◽  
Dara Dastan ◽  
Amir Nili-Ahmadabadi

Background: Pistacia atlantica kurdica has recently been shown to possess free radical scavenging ability. The current study aims to investigate the protective effect of this plant against cadmium-induced nephrotoxicity. Methods: Thirty-six rats were divided into 6 groups (6 in each), and treated as follows: group 1 received normal saline (control group), group 2 (positive control) received cadmium by drinking water (100 mg/ L/d), group 3 received 200 mg/kg of P. atlantica extract, and groups 4-6 received cadmium as well as 50, 100 and 200 mg/kg/d of P. atlantica extract (orally), respectively. After 2 weeks, oxidative damage and renal function markers were assayed by standard methods. Results: In cadmium group, a significant increase was observed in serum blood urea nitrogen (BUN) (P<0.01) and lipid peroxidation (LPO) level of renal tissue (P<0.001) and a remarkable decrease was found in total thiol molecules (TTM) of the kidney (P<0.001). Despite the decreased renal antioxidant capacity, these changes were not significant. P. atlantica extract improved the LPO, TTM, and histopathological changes in renal tissue. Conclusion: In this study, although the P. atlantica extract did not have a significant effect on cadmiuminduced renal dysfunction, it did improve the oxidative/antioxidant balance in renal tissue.


2007 ◽  
Vol 22 (5) ◽  
pp. 337-341 ◽  
Author(s):  
Célia Sperandéo Macedo ◽  
Mauro Masson Lerco ◽  
Sônia Maria Capelletti ◽  
Reinaldo José Silva ◽  
Daniela de Oliveira Pinheiro ◽  
...  

PURPOSE: To determine podocyte number and GBM thickness in diabetic rats either under glycemic control or without glycemic control at 6 and 12 months after diabetes induction. METHODS: 100 wistar rats weighing 200-300g were divided into 6 groups: Normal group (N6 and N12- 25 rats); Diabetic group (D6 and D12- 25 rats), diabetic treated group ( DT 6 and DT 12- 25 rats) on insulin 1,8- 3,0 IU/Kg associated with acarbose (50mg to 100g of food) daily mixed in chow. Alloxan was injected intravenously in a dose of 42 mg/Kg of weight. Body weight, waterintake, 24-h diuresis, glycemia and glucosuria were determined before induction, 7 and 14 days after induction and monthly thereafter. Treatment started at day 14. Three groups were sacrificed at 6 months (N6,D6, DT6) and 3 groups at 12 months (N12, D12, DT12) with the renal tissue being prepared for electron microscopy. RESULTS: Glycemia in DT6¨and in DT12 was significantly different from that in D6 and D12 rats and similar to that in N6 and N12 animals. The number of podocytes in DT6 was not different from that in N6 and D6 (median = 11); the number of podocytes in DT12 (median = 11) differed from that in D12 (median = 8), but not from that in N12 (median = 11). GBM thickness in D6 (0.18 micrometers) was lower than in D12 (0.29 micrometers); while in DT6 (0.16 micrometers) it was lower than in D6 (0.18 micrometers). In DT12 (0.26 micrometers), it was lower than in D12 (0.29 micrometers). CONCLUSION: The control of hyperglycemia prevented GBM thickening in early and late (12 mo) alloxan diabetic nephropathy and podocyte number reduction.


1959 ◽  
Vol 197 (4) ◽  
pp. 869-872 ◽  
Author(s):  
R. Hess ◽  
F. Gross

Using a histochemical method, moderately strong glucose-6-phosphate dehydrogenase activity can be demonstrated in the macula densa of the distal tubules in the normal rat kidney. In rats rendered hypertensive by overdosage with cortexone (DOC) and saline, this enzymatic activity was found to decrease almost to zero within 4 weeks. This change was more marked in unilaterally nephrectomized animals than in intact rats. Measured by bioassay, the renin content of kidney extracts from the same animals was found to decrease simultaneously with the loss of enzymatic activity in the macula cells. The reverse effect, a marked increase in activity of the macula densa, was obtained in adrenalectomized animals. It is suggested that both the macula densa cells and the juxtaglomerular apparatus are parts of a system which respond similarly to changes in sodium balance and which may be related to the formation of renin.


1994 ◽  
Vol 266 (2) ◽  
pp. F218-F226 ◽  
Author(s):  
R. Fernandez ◽  
M. J. Lopes ◽  
R. F. de Lira ◽  
W. F. Dantas ◽  
E. J. Cragoe Junior ◽  
...  

The cellular mechanism of luminal acidification (bicarbonate reabsorption) was studied in cortical distal tubules of rat kidney. The stopped-flow microperfusion technique was applied to early distal (ED) and late distal (LD) segments, perfused with bicarbonate Ringer solution to which specific inhibitors were added, to measure bicarbonate reabsorption [HCO3 flux (JHCO3)]. pH and transepithelial potential difference (Vt) were recorded by double-barreled H+ exchange resin/reference (1 M KCl) electrodes. Amiloride increased stationary pH and reduced Vt in both early and late segments. Hexamethylene-amiloride (HMA), a specific Na(+)-H+ exchange blocker, reduced JHCO3 in both segments (ED by 43.6 and LD by 40.3%) without affecting Vt. Benzamil, an Na(+)-channel blocker, reduced Vt by 75.9 in ED and 74.9% in LD but had no significant effect on acidification in both segments. The specific inhibitor of H(+)-ATPase, bafilomycin A1, inhibited LD JHCO3 at a concentration of 2 x 10(-7) M by 49%, but ED was inhibited by 24% only at 2 x 10(-6) M. Sch-28080, an inhibitor of gastric H(+)-K(+)-ATPase, reduced JHCO3 by 35% in LD of K(+)-depleted rats but not in control rats and had no effect on ED. These data indicate that, in ED, bicarbonate reabsorption is mediated mostly by Na(+)-H+ exchange. In LD, there is evidence for contribution of Na(+)-H+ exchange, vacuolar H(+)-ATPase, and H(+)-K(+)-ATPase (in K(+)-depleted rats) to bicarbonate reabsorption.


1971 ◽  
Vol 50 (3) ◽  
pp. 830-839 ◽  
Author(s):  
C. J. Tandler ◽  
A. L. Kierszenbaum

For localization of pyroantimonate-precipitable cations, rat kidney was fixed by perfusion with a saturated aqueous solution of potassium pyroantimonate (pH about 9.2, without addition of any conventional fixative). A remarkably good preservation of the tissue and cell morphology was obtained as well as a consistent and reproducible localization of the insoluble antimonate salts of magnesium, calcium, and sodium. All proximal and distal tubules and glomeruli were delimited by massive electron-opaque precipitates localized in the basement membrane and, to a lesser extent, in adjacent connective tissue. In the intraglomerular capillaries the antimonate precipitate was encountered in the basement membranes and also between the foot processes. In addition to a more or less uniform distribution in the cytoplasm and between the microvilli of the brush border, antimonate precipitates were found in all cell nuclei, mainly between the masses of condensed chromatin. The mitochondria usually contained a few large antimonate deposits which probably correspond to the so-called "dense granules" observed after conventional fixations.


1986 ◽  
Vol 250 (5) ◽  
pp. R753-R763 ◽  
Author(s):  
K. W. Beyenbach

This review attempts to give a retrospective survey of the available evidence concerning the secretion of NaCl and fluid in renal tubules of the vertebrate kidney. In the absence of glomerular filtration, epithelial secretory mechanisms, which to this date have not been elucidated, are responsible for the renal excretion of NaCl and water in aglomerular fish. However, proximal tubules isolated from glomerular fish kidneys of the flounder, killifish, and the shark also have the capacity to secrete NaCl and fluid. In shark proximal tubules, fluid secretion appears to be driven via secondary active transport of Cl. In another marine vertebrate, the sea snake, secretion of Na (presumably NaCl) and fluid is observed in freshwater-adapted and water-loaded animals. Proximal tubules of mammals can be made to secrete NaCl in vitro together with secretion of aryl acids. An epithelial cell line derived from dog kidney exhibits secondary active secretion of Cl when stimulated with catecholamines. Tubular secretion of NaCl and fluid may serve a variety of renal functions, all of which are considered here. The occurrence of NaCl and fluid secretion in glomerular proximal tubules of teleosts, elasmobranchs, and reptiles and in mammalian renal tissue cultures suggests that the genetic potential for NaCl secretion is present in every vertebrate kidney.


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