scholarly journals Pressure-diuresis in volume-expanded rats. Tubular reabsorption in superficial and deep nephrons.

Hypertension ◽  
1988 ◽  
Vol 12 (2) ◽  
pp. 177-183 ◽  
Author(s):  
R J Roman
Keyword(s):  
Tubular Reabsorption ◽  
Superficial And Deep Nephrons

Renal effects of nitric oxide synthesis inhibition in cirrhotic rats

1994 ◽  
Vol 267 (6) ◽  
pp. R1454-R1460 ◽  
Author(s):  
N. M. Atucha ◽  
J. Garcia-Estan ◽  
A. Ramirez ◽  
M. C. Perez ◽  
T. Quesada ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Renal Excretion ◽  
Renal Plasma Flow ◽  
Tubular Reabsorption ◽  
Nitric Oxide Synthesis ◽  
Important Mediator ◽  
Experimental Liver Cirrhosis ◽  
Endogenous Nitric Oxide ◽  
And Control ◽  
Experimental Liver

In the present study, we have characterized the renal response to inhibition of endogenous nitric oxide (NO) synthesis [intravenous NG-nitro-L-arginine methyl ester (L-NAME) for 3 h] in anesthetized cirrhotic rats, with (ASC) and without (CIR) ascites, at doses that do not change blood pressure (BP). Administration of L-NAME induced opposite effects on water (UV) and sodium (UNaV) excretion in cirrhotic and control animals. Infusion of 1 microgram.kg-1.min-1 of L-NAME in CIR (n = 5) decreased renal plasma flow (RPF) at the end of the 3-h period, whereas UV, UNaV, and glomerular filtration rate (GFR) were unaltered. In contrast, infusion of L-NAME at 10 micrograms.kg-1.min-1 in six more CIR increased UV and UNaV significantly by the 1st h, without changes in BP or GFR, and these parameters remained elevated throughout the experiment. Infusion of 1 microgram.kg-1.min-1 in ASC (n = 6) did not change BP or GFR but significantly enhanced UV and UNaV after the 1st h. These effects were prevented by pretreatment with L-arginine (0.1 mg.kg-1.min-1) in another group of ASC infused with 1 microgram.kg-1.min-1 of L-NAME. These results indicate that, in ASC and CIR cirrhotic rats, inhibition of NO synthesis at nonpressor does improves renal excretion of sodium and water via a decrease in tubular reabsorption. NO is an important mediator of the renal excretory and hemodynamic alterations of experimental liver cirrhosis.

Renal excretion of cephapirin and cephaloridine: Evidence for saturable tubular reabsorption

1979 ◽  
Vol 25 (6) ◽  
pp. 870-876 ◽  
Author(s):  
Annie Arvidsson ◽  
Olof Borgå ◽  
Gunnár Alvan
Keyword(s):  
Renal Excretion ◽  
Tubular Reabsorption

Lack of effect of chronic renal denervation on altered sodium reabsorption during increased ureteral pressure

1980 ◽  
Vol 58 (5) ◽  
pp. 477-483 ◽  
Author(s):  
D. R. Wilson ◽  
M. Cusimano ◽  
U. Honrath
Keyword(s):  
Isotonic Saline ◽  
Urine Osmolality ◽  
Tubular Reabsorption ◽  
Renal Nerves ◽  
Sodium Reabsorption ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Water Excretion ◽  
Renal Nerve Activity

The role of the renal nerves in the altered sodium reabsorption which occurs during increased ureteral pressure was studied using clearance techniques in anaesthetized rats undergoing diuresis induced by isotonic saline infusion. In rats with a sham denervated kidney, an ipsilateral increase in ureteral pressure to 20 cm H2O resulted in a marked and significant decrease in sodium and water excretion, increased fractional sodium reabsorption, and increased urine osmolality with no significant change in glomerular filtration rate. A similar significant ipsilateral increase in tubular reabsorption of sodium occurred in rats with chronically denervated kidneys during increased ureteral pressure. The changes in tubular reabsorption were rapidly reversible after return of ureteral pressure to normal. These experiments indicate that enhanced tubular reabsorption of sodium during an ipsilateral increase in ureteral pressure is not mediated by increased renal nerve activity. During the antinatriuresis of increased ureteral pressure there was a decrease in the fractional reabsorption of sodium from the opposite normal kidney. The role of the renal nerves in this compensatory change in function in the opposite kidney was studied in two further groups of animals. The renal response to a contralateral increase in ureteral pressure was similar in denervated and sham-denervated kidneys. The results indicate that altered renal nerve activity, through ipsilateral or contralateral renorenal reflexes, is not responsible for the changes in tubular reabsorption of sodium which occur during increased ureteral pressure induced by partial ureteral obstruction.

Evidence for Decreased Tubular Reabsorption of Calcium in Glucocorticoid-Treated Asthmatics

1987 ◽  
Vol 27 (4) ◽  
pp. 200-204 ◽  
Author(s):  
I.R. Reid ◽  
H.K. Ibbertson
Keyword(s):  
Tubular Reabsorption

scholarly journals Early post-transplantation hypophosphatemia is associated with elevated FGF-23 levels

2011 ◽  
Vol 164 (5) ◽  
pp. 839-847 ◽  
Author(s):  
Andrea Trombetti ◽  
Laura Richert ◽  
Karine Hadaya ◽  
Jean-Daniel Graf ◽  
François R Herrmann ◽  
...  
Keyword(s):  
Renal Transplantation ◽  
Tubular Reabsorption ◽  
Phosphate Metabolism ◽  
Multivariate Models ◽  
Intact Pth ◽  
Post Transplantation ◽  
Estimated Gfr ◽  
Renal Tubular Reabsorption ◽  
Renal Tubular ◽  
Fgf 23

BackgroundWe examined the hypothesis that high FGF-23 levels early after transplantation contribute to the onset of hypophosphatemia, independently of parathyroid hormone (PTH) and other factors regulating phosphate metabolism.MethodsWe measured serum phosphate levels (sPi), renal tubular reabsorption of Pi (TmPi/GFR), estimated GFR (eGFR), intact PTH (iPTH), calcitriol, intact (int) and C-terminal (Cter) FGF-23, dietary Pi intake and cumulative doses of glucocorticoids in 69 patients 12 days (95% confidence interval, 10–13) after renal transplantation.ResultsHypophosphatemia was observed in 43 (62%) of the patients 12 days after transplantation. Compared with non-hypophosphatemic subjects, their post-transplantation levels of intact and CterFGF-23 were higher (195 (108–288) vs 48 (40–64) ng/l, P<0.002 for intFGF-23; 205 (116–384) vs 81 (55–124) U/ml, P<0.002, for CterFGF-23). In all subjects, Cter and intFGF-23 correlated inversely with sPi (r=−0.35, P<0.003; −0.35, P<0.003, respectively), and TmPi/GFR (r=−0.50, P<0.001; −0.54, P<0.001, respectively). In multivariate models, sPi and TmPi/GFR were independently associated with FGF-23, iPTH and eGFR. Pre-transplant iPTH levels were significantly higher in patients developing hypophosphatemia after renal transplantation. Pre-transplant levels of FGF-23 were not associated with sPi at the time of transplantation.ConclusionIn addition to PTH, elevated FGF-23 may contribute to hypophosphatemia during the early post-renal transplant period.

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