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

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 radiofluoride in the dog

1960 ◽  
Vol 198 (4) ◽  
pp. 829-832 ◽  
Author(s):  
Curtis H. Carlson ◽  
W. D. Armstrong ◽  
Leon Singer ◽  
Lerner B. Hinshaw
Keyword(s):  
Plasma Concentration ◽  
Glomerular Filtration ◽  
Renal Excretion ◽  
Urine Volume ◽  
Urine Concentration ◽  
Tubular Reabsorption ◽  
Carrier Free ◽  
Renal Clearances ◽  
Concentration Ratios

Renal clearances of continuously infused radiofluoride were measured in 10 dogs in which a large part of the skeleton had been excluded from the system in order to produce a more constant plasma radiofluoride concentration. The results were evaluated to describe the factors of glomerular filtration and tubular reabsorption of fluoride under several conditions. The animals that received carrier-free radiofluoride infusions excreted urine with a mean radiofluoride concentration 3.4–14.5 times that of the plasma. The urine-to-plasma concentration ratios obtained with animals given a load of stable fluoride was 13.5–29.6. An increased urine volume resulted in a decreased tubular reabsorption of fluoride and the clearance was increased. Chlorothiazide increased radiofluoride excretion but decreased the urine concentration. The radiofluoride clearances were always less than the creatinine clearances but were 7.8–179 times the chloride clearances. The effect of chlorothiazide was to decrease the ratio of fluoride to chloride clearance by increasing chloride clearance more than fluoride clearance.

THE ACTION OF CORTICOSTEROIDS ON THE RENAL EXCRETION AND UTILIZATION OF CITRIC ACID

1964 ◽  
Vol 46 (3) ◽  
pp. 414-420 ◽  
Author(s):  
Helge Laake ◽  
Erling Kruge Brodwall
Keyword(s):  
Citric Acid ◽  
Steroid Hormones ◽  
Renal Excretion ◽  
Anabolic Steroids ◽  
Inhibitory Effect ◽  
Renal Tissue ◽  
Tubular Reabsorption ◽  
Enzyme Systems ◽  
Acid Clearance ◽  
Tubular Lumen

ABSTRACT During treatment with steroid hormones the tubular reabsorption of citric acid (cit.) increases, and the endogenous citric acid clearance is reduced. This is attributed to increased diffusion of citric acid from the tubular lumen to the renal tissue. With simultaneous administration of corticosteroids and anabolic steroids the tubular reabsorption of citric acid becomes normal. Steroid hormones block the renal synthesis of cit. and the renal utilization of cit. becomes identical with the amount of cit. reabsorbed in the tubules. Blockade of the synthesis of cit. is attributed to the inhibitory effect of steroid hormones on enzyme systems.

scholarly journals The role of tubular reabsorption in the renal excretion of bile acids

1977 ◽  
Vol 166 (1) ◽  
pp. 65-73 ◽  
Author(s):  
S Barnes ◽  
J L Gollan ◽  
B H Billing
Keyword(s):  
Bile Acids ◽  
Renal Excretion ◽  
Rat Kidney ◽  
Tubular Secretion ◽  
Tubular Reabsorption ◽  
Free Medium ◽  
Proximal Tubular ◽  
Protein Free Medium ◽  
Conjugated Bilirubin

1. The renal excretion of bile acids was studied in an isolated rat kidney preparation perfused with a protein-free medium. 2. Tubular reabsorption exceeded 95% for both non-sulphated and sulphated bile acids at filtered loads of less than 30 nmol/min. 3. At low filtered loads the reabsorption of taurocholate and taurochenodeoxycholate was almost complete. Efficient reabsorption of taurochenodeoxycholate was maintained over a wider range of filtered loads than for taurocholate. These observations suggest that active transport may occur. 4. At high filtered loads saturation of reabsorption of taurocholate and taurochenodeoxycholate did not occur, which indicates that passive diffusion is involved in reabsorption. 5. Active proximal-tubular secretion of bile acids was not demonstrated in competition experiments with p-aminohippurate. 6. The fractional reabsorption of taurocholate, chenodeoxycholate 3,7-disulphate and chenodeoxycholate 7-monosulphate was decreased by the addition of taurochenodeoxycholate to the perfusate, so that their renal excretion was enhanced. This interaction between the bile acids for reabsorption may explain the different composition of bile acids in urine compared with that in plasma in cholestasis in man. 7. Conjugated bilirubin decreased the fractional reabsorption of both taurocholate and taurochenodeoxycholate at low filtered loads (less than 30 nmol/min) but not at high filtered loads (400 nmol/min).

scholarly journals Dietary Magnesium, Not Calcium, Regulates Renal Thiazide Receptor

1999 ◽  
Vol 10 (3) ◽  
pp. 458-463
Author(s):  
DARRELL D. FANESTIL ◽  
RONALD H. HYDE ◽  
PATRICIA BLAKELY ◽  
DUKE A. VAUGHN
Keyword(s):  
Renal Excretion ◽  
Oral Intake ◽  
Tubular Reabsorption ◽  
Plasma Aldosterone ◽  
Ion Selective Electrodes ◽  
Ionized Magnesium ◽  
Saturation Binding ◽  
Dietary Magnesium ◽  
First Time ◽  
The Relationship

Abstract. This study reports for the first time a relationship between dietary Mg and the renal thiazide-sensitive Na-Cl cotransporter (TZR, measured by saturation binding with 3H-metolazone). Ion-selective electrodes measured plasma ionized magnesium (PMg+ +), calcium (PCa + +), and potassium (PK +). Restricting dietary Mg for 1 wk decreased PMg + + 18%, TZR 25%, and renal excretion of magnesium (UMg) and calcium (UCa) more than 50% without changing PCa + +, PK +, or plasma aldosterone. A low Mg diet for 1 d significantly decreased PMg + +, TZR, UMg and UCa. Return of dietary Mg after 5 d of Mg restriction restored PMg + + and TZR toward normal. In the control, Mg-deficient, and Mg-repleting animals, TZR correlated with PMg + + (r = 0.86) and with UMg (r = 0.87) but not UCa (r = 0.09). Increasing oral intake of Mg for 1 wk increased PMg + + 14%, TZR 32%, UMg 74%, and UCa more than fourfold without changing PCa + + or PK +. In contrast, increasing dietary Ca content from 0.02% to 1.91% did not change TZR, but increased UCa fivefold without changing PCa + +. Hormonal mediators (if any) involved in the relationship between dietary Mg and TZR remain to be elucidated, as does the relationship between TZR and tubular reabsorption of Mg.

scholarly journals THE CONTROL OF THE RENAL EXCRETION OF WATER

1942 ◽  
Vol 76 (4) ◽  
pp. 387-399 ◽  
Author(s):  
James A. Shannon
Keyword(s):  
Experimental Data ◽  
Diabetes Insipidus ◽  
Antidiuretic Hormone ◽  
Intravenous Infusion ◽  
Renal Excretion ◽  
Tubular Reabsorption ◽  
Posterior Pituitary ◽  
Hormone Administration ◽  
Renal Tubular Reabsorption ◽  
Renal Tubular

1. The administration of the posterior pituitary antidiuretic hormone by constant intravenous infusion has been used to examine the two characteristic actions of the hormone; namely, the facilitation of the active renal tubular reabsorption of water distally in the nephron and the inhibition of the renal tubular reabsorption of sodium proximally. 2. Experimental evidence was obtained which indicates that variations in the excretion of water and electrolyte involve the integration of these two actions with obscure variables which are discemible in the experimental data but are not subject to definition at this time. 3. Graded antidiuresis in the animal with diabetes insipidus, when normally hydrated, was only obtained in the range of 0.001 to 0.005 unit (pressor) per hour. This range of hormone administration was also found to be physiologically active in the normal animals. These observations together with others permit the placing of the normal rate of liberation of the antidiuretic hormone in a10 to 15 kilo dog in the range of 0.001 to 0.005 unit per hour.

Differential Determinants of Tubular Phosphate Reabsorption: Insights on Renal Excretion of Phosphates in Kidney Disease

2018 ◽  
Vol 47 (5) ◽  
pp. 300-303 ◽  
Author(s):  
Nahid Tabibzadeh ◽  
Romuald Mentaverri ◽  
Maïté Daroux ◽  
Rafik Mesbah ◽  
Alexia Delpierre ◽  
...  
Keyword(s):  
Kidney Disease ◽  
Iron Supplementation ◽  
Renal Excretion ◽  
Multivariable Analysis ◽  
Tubular Reabsorption ◽  
Phosphate Metabolism ◽  
Estimated Gfr ◽  
Phosphate Reabsorption ◽  
Renal Threshold ◽  
Tubular Phosphate Reabsorption

We assessed the tubular reabsorption of phosphate (TRP) and maximal renal threshold for phosphate reabsorption to glomerular filtration rate (TmPi/GFR) and their determinants in 64 stages 2–4 chronic kidney disease (CKD) patients in order to define the early changes in phosphate metabolism in CKD. In multivariable analysis, TmPi/GFR correlates were estimated GFR (eGFR), intact parathyroid hormone (iPTH), and hemoglobin (R2 = 0.417), while TRP correlates were eGFR, iPTH, 24-h phosphaturia, and calcitriol (R2 = 0.72). This suggests that TmPi/GFR and TRP, respectively, assess hemoglobin-phosphate and bowel-kidney phosphate regulation axis. Iron supplementation based on TmPi/GFR or earlier phosphate restriction based on TRP should be investigated in view of modifying clinical outcomes in CKD.

Effect of Vasopressin on the Renal Excretion of Phosphate in Man

1970 ◽  
Vol 39 (5) ◽  
pp. 687-692 ◽  
Author(s):  
A. J. Eisinger ◽  
N. F. Jones ◽  
M. A. Barraclough ◽  
R. R. McSwiney
Keyword(s):  
Creatinine Clearance ◽  
Renal Excretion ◽  
Tubular Reabsorption ◽  
Renal Tubules ◽  
Clearance Ratio ◽  
Phosphate Intake ◽  
Phosphate Excretion ◽  
The Common ◽  
Adenyl Cyclase System ◽  
Common Action

1. The effect of vasopressin on the tubular reabsorption of phosphate was studied in both water-restricted and water-loaded man at different baseline rates of phosphate excretion. The latter was varied by altering phosphate intake or by administering aluminium hydroxide to reduce phosphate absorption from the gut. 2. It was found that when phosphate excretion was high, vasopressin had no consistent effect on the phosphate/creatinine clearance ratio. However at low rates of phosphate excretion, vasopressin significantly increased the phosphate/creatinine clearance ratio, suggesting a decrease in net tubular reabsorption of phosphate. 3. This effect of vasopressin was also demonstrated in a patient with hypoparathyroidism, indicating that it is not mediated by release of parathormone. 4. It thus appears that vasopressin has a small parathormone-like effect on the renal tubules, which may result from the common action of both hormones on the adenyl cyclase system.

Renal Excretion of Radioiodide in Rats

1958 ◽  
Vol 193 (2) ◽  
pp. 379-385 ◽  
Author(s):  
N. S. Halmi ◽  
L. T. King ◽  
R. R. Widner ◽  
A. C. Hass ◽  
R. G. Stuelke
Keyword(s):  
Transport Mechanism ◽  
Renal Excretion ◽  
Competitive Inhibition ◽  
Sodium Thiosulfate ◽  
Tubular Reabsorption ◽  
Urine Flow ◽  
Male Rats ◽  
Renal Tubules ◽  
Sodium Salts ◽  
Active Transport Mechanism

Elimination of radioiodide by the kidney of adult male rats pretreated with a single dose of propylthiouracil was measured. Rats given water or isotonic saccharose served as controls. Renal clearance of radioiodide (CI131) was greatly enhanced (up to 100-fold) by the sodium salts of chloride, perchlorate, stable iodide, bromide and bicarbonate, and by choline iodide, but not by sodium thiosulfate. Under most conditions CI131 markedly exceeded the CCl and CNa of the same animals, which suggest that renal tubules are less permeable to iodide than to chloride or sodium. CI131/CNa varied greatly, its magnitude being dependent on the loading solution used. CI131 showed no correlation with urine flow or excretion of endogenous creatinine-like chromogen (UCrV) when groups receiving different treatments were compared. Both urine flow and UCrV showed only minor variations among these groups. Our findings are most easily explained by the hypothesis that tubular reabsorption of iodide filtered by the glomeruli involves, possibly in addition to a passive process, an active transport mechanism capable of saturation by iodide and (competitive?) inhibition by other anions.

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