THE MODE AND SITE OF THE RENAL ACTION OF PARATHYROID EXTRACT IN THE DOG

1959 ◽  
Vol 37 (1) ◽  
pp. 113-117 ◽  
Author(s):  
T. F. Nicholson
Keyword(s):  
Mode Of Action ◽  
Distal Tubule ◽  
Proximal Tubules ◽  
Similar Increase ◽  
Normal Kidney ◽  
Phosphate Excretion ◽  
Renal Action ◽  
Parathyroid Extract

When 20 U.S.P. units per kg of parathyroid extract were injected intravenously into dogs with unilateral distal tubular nephrosis, the phosphate excretion from the normal kidney increased significantly, but there was no change in the amount of phosphate excreted by the nephrotic kidney. In dogs with unilateral nephrosis affecting the first third or the last two thirds of the proximal tubules, parathyroid extract produced a similar increase in phosphate excretion by the normal and the nephrotic kidneys. It is concluded that the site of renal action of parathyroid extract is in the distal tubule and that its mode of action is to stimulate active excretion of phosphate.

THE MODE AND SITE OF THE RENAL ACTION OF PARATHYROID EXTRACT IN THE DOG

1959 ◽  
Vol 37 (1) ◽  
pp. 113-117 ◽  
Author(s):  
T. F. Nicholson
Keyword(s):  
Mode Of Action ◽  
Distal Tubule ◽  
Proximal Tubules ◽  
Similar Increase ◽  
Normal Kidney ◽  
Phosphate Excretion ◽  
Renal Action ◽  
Parathyroid Extract

When 20 U.S.P. units per kg of parathyroid extract were injected intravenously into dogs with unilateral distal tubular nephrosis, the phosphate excretion from the normal kidney increased significantly, but there was no change in the amount of phosphate excreted by the nephrotic kidney. In dogs with unilateral nephrosis affecting the first third or the last two thirds of the proximal tubules, parathyroid extract produced a similar increase in phosphate excretion by the normal and the nephrotic kidneys. It is concluded that the site of renal action of parathyroid extract is in the distal tubule and that its mode of action is to stimulate active excretion of phosphate.

Nephron heterogeneity of phosphate reabsorption: effect of parathyroid hormone

1984 ◽  
Vol 246 (2) ◽  
pp. F155-F158
Author(s):  
A. Haramati ◽  
J. A. Haas ◽  
F. G. Knox
Keyword(s):  
Parathyroid Hormone ◽  
Proximal Tubule ◽  
Distal Tubule ◽  
Proximal Tubules ◽  
Loop Of Henle ◽  
Phosphate Reabsorption ◽  
Phosphate Excretion ◽  
Before And After ◽  
Superficial And Deep Nephrons ◽  
Nephron Heterogeneity

We evaluated the response of superficial and deep nephron proximal tubules to PTH in thyroparathyroidectomized (TPTX) rats fed a normal phosphate diet (0.7%). As phosphate reabsorption is not detectable in the ascending limb of the loop of Henle, fractional phosphate delivery (FDPi%) to the superficial early distal tubule and papillary loop of Henle reflects delivery from superficial and deep nephron proximal tubules, respectively. Re-collection micropuncture experiments were performed in nine acutely TPTX rats before and after the infusion of PTH (33 U/kg bolus; 1 U X kg-1 X min-1). In response to PTH, fractional phosphate excretion increased from 3.3 to 26.2% (P less than 0.05). FDPi% was less from the deep than from the superficial proximal tubule (5.7 vs. 15.7%, P less than 0.05) prior to PTH, indicating enhanced phosphate reabsorption by deep compared with superficial proximal tubules. During PTH infusion, FDPi% was increased in both nephron groups compared with control (P less than 0.05), but there were no differences in phosphate delivery between deep (28.0%) and superficial (29.7%) proximal tubules. We conclude that in acutely volume-expanded TPTX rats, infusion of a pharmacologic dose of PTH decreases phosphate reabsorption in both superficial and deep nephrons. Furthermore, the heterogeneity of FDPi% from deep compared with superficial proximal tubules seen in TPTX rats is absent during PTH infusion.

Adaptation of deep and superficial nephrons to changes in dietary phosphate intake

1983 ◽  
Vol 244 (3) ◽  
pp. F265-F269 ◽  
Author(s):  
A. Haramati ◽  
J. A. Haas ◽  
F. G. Knox
Keyword(s):  
Proximal Tubule ◽  
Distal Tubule ◽  
Proximal Tubules ◽  
Loop Of Henle ◽  
Phosphate Reabsorption ◽  
Phosphate Intake ◽  
Phosphate Excretion ◽  
Dietary Phosphate ◽  
Renal Phosphate Excretion ◽  
High Phosphate

Dietary phosphate intake is now recognized to be a primary regulator of renal phosphate excretion. However, the nephron sites involved in the adaptation to changes in dietary phosphate are unclear. We tested the hypothesis that deep and superficial nephrons respond differently to changes in dietary phosphate by comparing fractional phosphate delivery (FDP%) from proximal tubules of both nephron populations. Because phosphate reabsorption is not detectable in the ascending loop of Henle, FDP% to the superficial early distal tubule and papillary loop of Henle reflect delivery from superficial and deep nephron proximal tubules, respectively. Micropuncture experiments were performed in 17 acutely TPTX rats fed either a low (0.07%) or a high (1.8%) phosphate diet for 4 days prior to the experiment. In low phosphate diet, fractional phosphate excretion was 0.93 +/- 0.26%. FDP% was 7.5 +/- 0.5 and 9.1 +/- 2.2% from superficial and deep nephron proximal tubules, respectively (P greater than 0.05). In high phosphate diet, fractional phosphate excretion was 29.6 +/- 5.0%. FDP% was significantly greater from superficial proximal tubules, 33.9 +/- 4.6%, compared with that from deep nephron proximal tubules, 14.0 +/- 2.7% (P less than 0.05). We conclude that significant adaptation of phosphate reabsorption in response to changes in dietary phosphate intake occurs in the superficial but not in the deep nephron proximal tubule in acutely TPTX volume-expanded rats. In addition, the presence of distal phosphate reabsorption was not evident in high phosphate diet but must occur in low phosphate diet.

THE EFFECT OF DAMAGE TO VARIOUS PARTS OF THE RENAL TUBULE ON THE EXCRETION OF PHOSPHATE BY THE DOG'S KIDNEY

1959 ◽  
Vol 37 (1) ◽  
pp. 103-111 ◽  
Author(s):  
T. F. Nicholson ◽  
G. W. Shepherd
Keyword(s):  
Proximal Tubule ◽  
Mercuric Chloride ◽  
Renal Tubule ◽  
Potassium Dichromate ◽  
Left Kidney ◽  
Distal Tubule ◽  
Proximal Tubules ◽  
Sodium Tartrate ◽  
Phosphate Excretion ◽  
Distal Tubules

The first third of the proximal tubules of the left kidney in dogs was damaged by the injection of 2.5 mg% potassium dichromate, the last two thirds by the injection of 0.5% sodium tartrate, and the distal tubules by the retrograde injection up the ureter of 0.05% mercuric chloride. Damage to the first third of the proximal tubule resulted in marked increase in phosphate excretion. Damage to the last two thirds of the proximal tubule had no significant effect on the output of phosphate. When the distal tubule was damaged the excretion of phosphate was greatly reduced. The results indicate that phosphate is reabsorbed in the first third of the proximal tubule and actively excreted by the distal tubule.

THE EFFECT OF DAMAGE TO VARIOUS PARTS OF THE RENAL TUBULE ON THE EXCRETION OF PHOSPHATE BY THE DOG'S KIDNEY

1959 ◽  
Vol 37 (1) ◽  
pp. 103-111 ◽  
Author(s):  
T. F. Nicholson ◽  
G. W. Shepherd
Keyword(s):  
Proximal Tubule ◽  
Mercuric Chloride ◽  
Renal Tubule ◽  
Potassium Dichromate ◽  
Left Kidney ◽  
Distal Tubule ◽  
Proximal Tubules ◽  
Sodium Tartrate ◽  
Phosphate Excretion ◽  
Distal Tubules

The first third of the proximal tubules of the left kidney in dogs was damaged by the injection of 2.5 mg% potassium dichromate, the last two thirds by the injection of 0.5% sodium tartrate, and the distal tubules by the retrograde injection up the ureter of 0.05% mercuric chloride. Damage to the first third of the proximal tubule resulted in marked increase in phosphate excretion. Damage to the last two thirds of the proximal tubule had no significant effect on the output of phosphate. When the distal tubule was damaged the excretion of phosphate was greatly reduced. The results indicate that phosphate is reabsorbed in the first third of the proximal tubule and actively excreted by the distal tubule.

P0894OBESITY IMPAIRS THE ACUTE RESPONSE TO AN ORAL PHOSPHATE CHALLENGE

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Mandy Turner ◽  
Christine White ◽  
Patrick Norman ◽  
Corinne Babiolakis ◽  
Michael Adams ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
High Risk ◽  
Kidney Function ◽  
Area Under The Curve ◽  
Fractional Excretion ◽  
Low Risk ◽  
Normal Kidney ◽  
Phosphate Excretion ◽  
Fractional Excretion Of Phosphate ◽  
Age And Sex

Abstract Background and Aims T Obesity is an increasing health problem world-wide. People who are overweight or obese are at greater risk of developing chronic diseases including cardiovascular disease (CVD). Factors associated with dysregulated phosphate metabolism have been linked to the presence of vascular calcification in people with type 2 diabetes (T2D) with normal kidney function. Insulin resistance and abdominal obesity are associated with increased circulating levels of phosphaturic hormones including fibroblast growth factor 23 (FGF-23) and parathyroid hormone (PTH). Abnormalities in phosphate regulation may not be reflected in single circulating measurements of serum phosphate, but can be revealed by the acute circulating and mineral response to an oral challenge of phosphate. The aim of this study was to determine if obesity and insulin resistance impact the acute capacity to excrete an oral phosphate challenge. Method Community-dwelling people (N=78) free of T2D and symptomatic CVD (∼10 males and ∼10 females from each decade between 40 and 80 years) with normal kidney function were recruited from Kingston, Ontario, Canada. Following a 12-hour fast, participants consumed a 1250 mg phosphate drink (sodium phosphate) where blood and urine were collected at baseline, 1, 2 and 3 hours following the oral challenge. Participants with a high-risk metabolic profile characterized by an elevated waist-to-height ratio (WHtR) (> 0.58) were matched by age and sex to participants with a low risk WHtR (<0.5). Results The results reveal a significant impact of obesity on phosphate excretion in response to an oral phosphate challenge. There was an association between WHtR ratio and the level of iFGF-23 (R=-0.34 p<0.01) but not PTH. After adjustment for age and sex, WHtR ratio was inversely correlated with urinary phosphate excretion in response to the phosphate challenge (R=-0.29, p=0.02) and the change in fractional excretion of phosphate (r=-0.34, p=0.007). From the larger cohort, an age- and sex- matched subset was selected for 12 high risk and 12 low risk metabolic profiles with WHtR of 0.66±0.02 and 0.46±0.01, respectively. Kidney function was the same between the two groups (eGFR 92.3±13.1 versus 95.8±13.6 ml/min/1.73m2 respectively) but high risk participants had significantly higher homeostatic model assessment of insulin resistance (HOMA-IR) (1.61±0.81 versus 0.68±0.3, p<0.01). Participants with a high risk metabolic profile had a greater increase in serum phosphate from baseline (29% increase in the area under the curve, p=0.04) and a significantly blunted increase in the fractional excretion of phosphate in response to the oral phosphate challenge (35% reduction in area under the curve [AUC], p=0.03) compared to the matched low risk profile participants. Conclusion Overweight/obese individuals demonstrate impaired response to an oral phosphate challenge, whereby phosphate excretion was impaired and there was increased exposure to new circulating phosphate. An impaired acute phosphate response may contribute to the initiation or propagation of vascular calcification. Dysregulated phosphate homeostasis may be an under-recognized cardiovascular risk factor in obese people that could be modified by diet and weight loss. Whether insulin enhances renal phosphate reabsorption requires further study.

scholarly journals Endopeptidases (kininases) are able to hydrolyze kinins in tubular fluid along the rat nephron

1999 ◽  
Vol 277 (1) ◽  
pp. F66-F74 ◽  
Author(s):  
D. E. Casarini ◽  
M. A. Boim ◽  
R. C. R. Stella ◽  
N. Schor
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Proximal Tubule ◽  
Physiological Role ◽  
Distal Tubule ◽  
Neutral Endopeptidase ◽  
Prolyl Endopeptidase ◽  
Proximal Tubules ◽  
Converting Enzyme ◽  
Distal Nephron ◽  
Distal Tubules

The activities of serine endopeptidase, prolyl endopeptidase and neutral endopeptidase were determined in tubular fluid collected from several portions of the rat nephron as well as in urine. The enzyme activities were measured by HPLC using bradykinin (BK) as substrate. Free residual peptides of BK obtained by the action of these enzymes on the locally produced BK were also determined. The endopeptidase activities were found to be present throughout the nephron. Equimolar fragments of BK were detected in the early proximal tubule (Arg1-Pro7, Phe8-Arg9, Arg1-Gly4, Phe5-Arg9, and BK), late proximal tubule (Arg1-Phe5, Arg1-Pro7, Gly4-Pro7, Gly4-Arg9, and BK), late distal tubule (Arg1-Gly4, Phe5-Arg9, Arg1-Phe5, Ser6-Arg9, Gly4-Arg9, BK, and [des-Arg9]BK) and urine (Phe8-Arg9, Phe5-Arg9, Arg1-Phe5, Ser6-Arg9, Arg1-Pro7, Gly4-Pro7, Gly4-Arg9, BK, and [des-Arg9]BK). Our data suggest that the endopeptidases and exopeptidases are secreted by the nephron. Early proximal tubules secrete angiotensin converting enzyme and neutral endopeptidase, differing from late distal tubules that produce prolyl endopeptidase, serine endopeptidase, carboxypeptidase, and also neutral endopeptidase. All enzymes detected along the rat nephron were found in the urine. The existence of endopeptidases and carboxypeptidase in the distal nephron may have a potential physiological role in the inactivation of the kinins formed by kallikrein in the kidney and also in the inactivation of additional peptides other than BK.

Renal handling of gentamicin by the Munich-Wistar rat

1981 ◽  
Vol 241 (6) ◽  
pp. F645-F648
Author(s):  
A. U. Sheth ◽  
H. O. Senekjian ◽  
H. Babino ◽  
T. F. Knight ◽  
E. J. Weinman
Keyword(s):  
Rat Kidney ◽  
Extracellular Fluid ◽  
Distal Tubule ◽  
Wistar Rat ◽  
Significant Degree ◽  
Proximal Tubules ◽  
Loop Of Henle ◽  
Renal Handling ◽  
Isotonic Sodium Chloride ◽  
Nephron Heterogeneity

Free-flow micropuncture studies were performed in the Munich-Wistar rat to determine the nephron sites of gentamicin transport. The rats were infused with radiolabeled gentamicin and were volume-expanded with either isotonic sodium chloride or sodium bicarbonate. The fractional delivery of ultrafilterable gentamicin (FD) out of the superficial proximal tubule averaged 75% in both groups of animals. FD to the superficial distal tubule averaged 58.1 +/- 2.1% in saline-infused and 91.6 +/- 5.3% in bicarbonate-infused animals. FD to Henle's loop was 118.2 +/- 8.8 and 124.3 +/- 8.1% in saline- and bicarbonate-infused animals, respectively. FD to the base and tip of the papilla was not significantly different between the two groups and averaged 97.3 +/- 2.9 and 96.1 +/- 3.0% in the saline-infused and 100.5 +/- 2.6 and 94.3 +/- 2.8% in the bicarbonate-infused animals. FD to the base of the papilla was significantly lower than that to the loop of Henle in both groups. These studies indicate that gentamicin undergoes net reabsorption in juxtamedullary proximal tubules. Expansion of the extracellular fluid volume with saline or bicarbonate results in differing rates of gentamicin delivery to the superficial distal tubule but not to the base of the papilla. These findings suggest a significant degree of nephron heterogeneity for gentamicin transport in the rat kidney.

Nicotinamide restores phosphaturic effect of PTH and calcitonin in phosphate deprivation

1982 ◽  
Vol 242 (5) ◽  
pp. F447-F452 ◽  
Author(s):  
T. J. Berndt ◽  
J. D. Pfeifer ◽  
F. G. Knox ◽  
S. A. Kempson ◽  
T. P. Dousa
Keyword(s):  
Nicotinamide Adenine Dinucleotide ◽  
Intraperitoneal Administration ◽  
Phosphate Transport ◽  
Tubular Reabsorption ◽  
Proximal Tubules ◽  
Dibutyryl Camp ◽  
Cellular Regulation ◽  
Phosphate Excretion ◽  
Camp Generation ◽  
Clearance Studies

Results of previous studies suggest a potentially important role for nicotinamide adenine dinucleotide (NAD) in the cellular regulation of phosphate transport by the renal proximal tubules. The present clearance studies were performed to evaluate whether intraperitoneal administration of nicotinamide, a precursor of NAD and inhibitor of NAD catabolism, would not only increase phosphate excretion but also restore the phosphaturic response to parathyroid hormone (PTH) in rats fed a low phosphate diet. Rats fed a low phosphate diet were resistant to the phosphaturic effect of PTH, calcitonin, and dibutyryl cAMP (DBcAMP) in spite of the fact that all three agents elicited an increase in the urinary excretion of cAMP. Administration of nicotinamide to rats fed a low phosphate diet increased renal cortical NAD levels, increased phosphate excretion, partially restored the phosphaturic effect of PTH and DBcAMP, and completely restored the phosphaturic response to calcitonin. We conclude that nicotinamide restores the phosphaturic effect of PTH and calcitonin in rats fed a low phosphate diet by acting at a cellular step subsequent to cAMP generation to inhibit tubular reabsorption of phosphate.

scholarly journals Immunocytochemical demonstration of vasopressin binding in rat kidney.

1990 ◽  
Vol 38 (1) ◽  
pp. 7-12 ◽  
Author(s):  
J M Fadool ◽  
S K Aggarwal
Keyword(s):  
Considerable Increase ◽  
Rat Kidney ◽  
Proximal Tubules ◽  
Normal Kidney ◽  
Renal Papilla ◽  
Collecting Ducts ◽  
Immunoperoxidase Labeling ◽  
Convoluted Tubules ◽  
Similar Decrease

We investigated the immunoperoxidase demonstration of vasopressin (VSP) bound to paraffin-embedded sections of rat kidney and the effects of various fixatives. Slices of rat kidney from normal and 4-day water-deprived rats were incubated with 10(-7) M VSP, fixed, and embedded in paraffin. Hydrated sections of these tissues were again incubated with 10(-7) M VSP or 10(-7) M VSP and 10(-5) M oxytocin (OXY). VSP bound to the sections was demonstrated using rabbit anti-Arg8 VSP antiserum and peroxidase-labeled second antibody. In sections of kidney from both normal and water-deprived rats, immunoperoxidase labeling was most intense in the renal papilla and was restricted to the cells of the ducts of Bellini and loops of Henle. In the medulla, the collecting ducts and medullary thick ascending limbs of Henle were moderately stained. In the normal kidney sections there was no staining of the proximal tubules, distal convoluted tubules (DCT), and only slight staining of the cortical collecting ducts (CCD). However, in the water-deprived rats there was a considerable increase in the staining of the DCT and CCD. Simultaneous incubation in OXY and VSP resulted in reduced immunoperoxidase labeling of the tubules. Omission of VSP incubation led to a similar decrease in stain intensity, indicating a specificity for the sites of VSP binding. This technique allows the identification of cells responsible for the binding of VSP in the kidney.

Sign in / Sign up

Export Citation Format

Share Document