scholarly journals Dopamine enhances the phosphaturic response to parathyroid hormone in phosphate-deprived rats.

1992 ◽  
Vol 2 (9) ◽  
pp. 1423-1429
Author(s):  
J Isaac ◽  
T J Berndt ◽  
S L Chinnow ◽  
G M Tyce ◽  
T P Dousa ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Fractional Excretion ◽  
Phosphate Transport ◽  
Dopamine Synthesis ◽  
Dopamine Infusion ◽  
Phosphate Deprivation ◽  
Dietary Phosphate ◽  
Urinary Dopamine ◽  
Fractional Excretion Of Phosphate ◽  
High Phosphate

Phosphate deprivation results in a resistance to the phosphaturic effect of parathyroid hormone. Dopamine is phosphaturic and is synthesized by kidney proximal tubule, the nephron subsegment where parathyroid hormone inhibits phosphate transport. Thus, to test the hypothesis that phosphate deprivation is associated with low intrarenal dopamine synthesis and that dopamine infusion will overcome the resistance to the phosphaturic response to parathyroid hormone, the following study was performed. The effect of dietary phosphate intake on intrarenal dopamine synthesis, as reflected by urinary dopamine excretion, was determined. Rats were placed in metabolic cages (N = 5) and were fed a low-phosphate diet (0.07% Pi) for 4 days and then a high-phosphate diet (1.8% Pi) for 4 days. Twenty-four-hour urinary dopamine excretion was significantly lower in rats fed a low-phosphate diet (2.53 +/- 0.06 versus 4.10 +/- 0.30 micrograms/day). Further, the effect of dopamine infusion on the blunted phosphaturic response to parathyroid hormone was studied in rats fed a low-phosphate diet for 1, 2, and 3 days. Control clearances were taken 2 h after thyroparathyroidectomy; then, parathyroid hormone (33 U/kg plus 1 U/kg/min), dopamine (25 micrograms/kg/min), or parathyroid hormone plus dopamine were infused for 60 min. Changes in the fractional excretion of phosphate were significantly greater in rats fed a low-phosphate diet infused with parathyroid hormone plus dopamine than in rats fed a low-phosphate diet infused with parathyroid hormone alone (delta 27.9 +/- 5.8 versus 11.2 +/- 2.6% for day 1; 28.4 +/- 1.4 versus 7.1 +/- 3.6% for day 2; and 10.7 +/- 2.8 versus -0.2 +/- 0.2% for day 3; N = 5 for all groups).(ABSTRACT TRUNCATED AT 250 WORDS)

Tubular capacity of phosphate transport in phosphate-deprived rats: effects of nicotinamide and PTH

1983 ◽  
Vol 244 (2) ◽  
pp. F178-F184 ◽  
Author(s):  
A. Haramati ◽  
F. G. Knox
Keyword(s):  
Parathyroid Hormone ◽  
Phosphate Transport ◽  
Phosphate Deprivation ◽  
Phosphate Excretion ◽  
Dietary Phosphate ◽  
Lower Maximum ◽  
Filtered Load

The present study tested the hypothesis that nicotinamide and/or parathyroid hormone (PTH) would reverse the resistance of phosphate-deprived rats to the phosphaturic effects of phosphate infusions by reducing the tubular capacity for phosphate transport. The response to progressively increasing rates of phosphate infusion (1, 2, and 3 mumol/min) was evaluated in thyroparathyroidectomized (TPTX) rats fed low phosphate diet (0.07%) for 4 days and treated with either vehicle or nicotinamide 2 h before the experiment. Following phosphate infusions, phosphate excretion was unchanged in vehicle-treated rats but increased progressively in nicotinamide-treated rats to 60% of the final rate of infusion. In a second series conducted in the presence of exogenous PTH, vehicle-treated rats responded to phosphate infusions by increasing phosphate excretion to 80-90% of the rate of infusion. In the presence of both nicotinamide and PTH, the rate of phosphate excretion matched the rate of infusion. Vehicle-treated rats displayed the highest reabsorptive rates without reaching a transport maximum, whereas a lower maximum reabsorptive rate was evident in nicotinamide-treated rats. However, in both groups given PTH, not only was the transport maximum lower but it declined with further increases in filtered load. We conclude that nicotinamide and PTH reverse the effects of dietary phosphate deprivation by decreasing the tubular capacity for phosphate transport.

Propranolol restores phosphaturic effect of PTH in short-term phosphate deprivation

1990 ◽  
Vol 258 (1) ◽  
pp. R120-R123
Author(s):  
A. Rybczynska ◽  
A. Hoppe ◽  
F. G. Knox
Keyword(s):  
Parathyroid Hormone ◽  
Fractional Excretion ◽  
Adrenergic System ◽  
Sprague Dawley ◽  
Short Term ◽  
Phosphate Deprivation ◽  
Sprague Dawley Rats ◽  
Complete Resistance ◽  
Fractional Excretion Of Phosphate

Phosphate deprivation causes a resistance to the phosphaturic effect of parathyroid hormone (PTH). The present study evaluated the role of the beta-adrenergic system in this resistance phenomenon. In clearance experiments performed on acutely thyroparathyroidectomized male Sprague-Dawley rats, the phosphaturic response to PTH was determined in the presence and absence of propranolol in rats fed a low-phosphate diet (LPD) for 0.5, 1, 2, 3, or 4 days. Fractional excretion of phosphate (FEPi) in control rats fed a normal-phosphate diet (NPD) increased from 4.37 +/- 1.6 to 38.5 +/- 3.4% in response to PTH infusion. Propranolol did not change FEPi in NPD animals in the absence or in the presence of PTH (2.0 +/- 1.1 vs. 36.7 +/- 1.6%). LPD resulted in a gradual decrease in the phosphaturic response to PTH infusion as compared with NPD animals. PTH increased FEPi to 24.2 +/- 6.0% after one-half day of LPD, but when the infusion was supplemented with propranolol, PTH increased FEPi to 38.0 +/- 4.7%, similar to that in NPD animals. In the group fed LPD for one day, PTH increased FEPi to 16.9 +/- 4.3%, whereas in the presence of propranolol FEPi was restored to a similar level as in the NPD group (36.0 +/- 5.9%). Two days of LPD markedly decreased FEPi in response to PTH to 7.9 +/- 3.8% as compared with NPD rats, and propranolol infusion did not change this value significantly. Three and 4 days of LPD induced complete resistance to the phosphaturic effect of PTH in the presence as well as in the absence of propranolol.(ABSTRACT TRUNCATED AT 250 WORDS)

Renal Phosphate Adaptation in Uraemic Dogs with a Remnant Kidney

1981 ◽  
Vol 60 (3) ◽  
pp. 273-282 ◽  
Author(s):  
S.-F. Wen ◽  
R. W. Stoll
Keyword(s):  
Renal Failure ◽  
Parathyroid Hormone ◽  
Chronic Renal Failure ◽  
Volume Expansion ◽  
Extracellular Volume ◽  
Fractional Excretion ◽  
Phosphate Transport ◽  
Extracellular Volume Expansion ◽  
Fractional Excretion Of Phosphate ◽  
Remnant Kidney

1. Clearance and micropuncture studies were performed in 27 dogs made uraemic by segmental infarction to examine the factors responsible for phosphate adaptation in chronic renal failure. 2. The animals were studied before and after extracellular volume expansion to 10% of body weight in the presence and absence of parathyroid glands. The results were compared with 19 normal dogs studied under similar experimental conditions. 3. In the dogs with a remnant kidney and intact parathyroids adaptation of phosphate transport was evident, with a high fractional excretion of phosphate. Thyroparathyroidectomy 3 days before study in the dogs with a remnant kidney and moderate renal failure reduced fractional excretion of phosphate to near normal values, indicating a major role of parathyroid hormone in phosphate adaptation. Extracellular volume expansion in these thyroparathyroidectomized uraemic dogs led to an exaggerated phosphaturic response with fractional excretion of phosphate returning towards the value in the uraemic dogs with intact parathyroid glands. Thus acute extracellular volume expansion could also contribute to the increase in fractional phosphate excretion, but extracellular volume probably plays a relatively minor role in the adaptation of phosphate excretion. 4. With more advanced renal failure fractional excretion of phosphate remained high, even after thyroparathyroidectomy, indicating that parathyroid hormone-independent factors become important for phosphate adaptation in the advanced stage of renal failure. The nature of parathyroid hormone-independent changes in fractional phosphate reabsorption in chronic renal failure remains unknown. 5. Proximal tubular fluid/plasma ultrafiltrate phosphate ratios were high in all groups of dogs with a remnant kidney regardless of thyroparathyroidectomy or the degree of renal failure. The non-specific nature of the proximal tubule pattern of phosphate transport indicates that phosphate adaptation is primarily determined by alterations in phosphate transport at a site distal to the proximal convoluted tubule. Alternatively, deep nephrons may play a greater role in determination of the overall phosphate adaptation in the chronically diseased kidney.

Resistance to the phosphaturic effect of parathyroid hormone in the hamster

1979 ◽  
Vol 237 (3) ◽  
pp. F175-F181
Author(s):  
C. A. Harris ◽  
J. F. Seely
Keyword(s):  
Parathyroid Hormone ◽  
Fractional Excretion ◽  
Free Access ◽  
Calcium Excretion ◽  
Renal Tubular Cell ◽  
Acid Base ◽  
Significant Difference ◽  
Renal Tubular ◽  
Fractional Excretion Of Phosphate ◽  
Access To Food

The renal effects of parathyroid hormone (PTH) and dibutyryl 3'5'-cyclic AMP (DBcAMP) were studied in thyroparathyroidectomized hamsters. The hamsters were permitted free access to food and water or fasted for 16 h. PTH caused a phosphaturia in the fed hamster (fractional excretion of phosphate (FEPO4) increased from 5.8 +/- 1.3 to 27.4 +/- 4.6%, P less than 0.001) but not in the fasted hamster (from 9.9 +/- 2.5 to 12.4 +/- 2.5%, NS), whereas calcium excretion decreased significantly in both groups. There was no significant difference in blood acid-base or phosphate levels between the two groups. Insulin did not restore the phosphaturic response to PTH (FEPO4 from 7.7 +/- 2.6 to 5.3 +/- 1.7%), whereas phosphate or NH4Cl infusion did, FEPO4 increasing from 20.9 +/- 3.1 to 38.1 +/- 5.4% (P less than 0.02) and from 19.5 +/- 3.8 to 39.0 +/- 7.5%, respectively. DBcAMP caused a phosphaturia both in the fasted (from 9.6 +/- 2.7 to 20.1 +/- 4.5%, P less than 0.01) and fed (from 2.5 +/- 0.5 to 10.7 +/- 1.5%, P less than 0.02) hamster. A fasting state of up to 64 h did not produce resistance to PTH in the rat. It is concluded that fasting produces resistance to the phosphaturic but not the calcium-retaining effects of PTH in the hamster. The resistance may occur, at least partly, prior to the production of cAMP within the renal tubular cell.

Phosphate excretion in uremic rats: effects of parathyroidectomy and phosphate restriction

1985 ◽  
Vol 248 (2) ◽  
pp. F175-F182
Author(s):  
E. Kraus ◽  
G. Briefel ◽  
L. Cheng ◽  
B. Sacktor ◽  
D. Spector
Keyword(s):  
Fractional Excretion ◽  
Tubular Reabsorption ◽  
Sprague Dawley ◽  
Dietary Regimen ◽  
Phosphate Excretion ◽  
Sprague Dawley Rats ◽  
Dietary Phosphate ◽  
Phosphate Loading ◽  
Fractional Excretion Of Phosphate ◽  
Renal Phosphate Excretion

As progressive renal failure develops, phosphate excretion per functioning nephron increases, thus preserving homeostasis. To test whether dietary phosphate supply might contribute to the regulation of renal phosphate excretion in the uremic setting, groups of male Sprague-Dawley rats that were either parathyroidectomized (PTX) or sham PTX (S-PTX) and either five-sixths nephrectomized (Nx) or sham Nx (S-Nx) were studied following a 4-wk dietary regimen consisting of 0.1 or 0.7% phosphate. For Nx rats fed the 0.7% phosphate diet the fractional excretion of phosphate (FEPi) was enhanced (47 +/- 6 vs. 21 +/- 3%) and the maximum tubular reabsorption of phosphate per milliliter GFR (TmPi/GFR) was suppressed (1.65 +/- 0.19 vs. 2.33 +/- 0.19 mumol/ml). FEPi was unchanged by PTX in these Nx animals (42 +/- 6 vs. 47 +/- 6%). TmPi/GFR remained suppressed in PTX, NX animals when compared with S-Nx, PTX controls (3.38 +/- 0.33 vs. 5.07 +/- 0.41 mumol/ml). For rats fed the 0.1% phosphate diet Nx did not affect TmPi/GFR in either S-PTX (5.40 +/- 0.43 vs. 4.97 +/- 0.34 mumol/ml) or PTX (7.03 +/- 0.23 vs. 6.98 +/- 0.21 mumol/ml) animals. For both S-Nx and Nx animals the effects of PTX and dietary phosphate restriction on TmPi/GFR were independent and additive. In all groups of animals, tubular reabsorption of phosphate per milliliter GFR (TRPi/GFR) dropped acutely with continued infusion of phosphate once TmPi/GFR was achieved. Thus, a resetting of TRPi/GFR occurs among Nx rats in response to both chronic dietary phosphate deprivation and acute intravenous phosphate loading.(ABSTRACT TRUNCATED AT 250 WORDS)

Mechanisms of hypophosphatemia in humans with heatstroke

1991 ◽  
Vol 71 (1) ◽  
pp. 328-332 ◽  
Author(s):  
A. Bouchama ◽  
A. Cafege ◽  
W. Robertson ◽  
S. al-Dossary ◽  
A. el-Yazigi
Keyword(s):  
Parathyroid Hormone ◽  
Hormone Level ◽  
Fractional Excretion ◽  
Tubular Dysfunction ◽  
Plasma Phosphate ◽  
Normal Range ◽  
Renal Threshold ◽  
Blood Ph ◽  
Glomerular Filtrate ◽  
Fractional Excretion Of Phosphate

Hypophosphatemia is common in heatstroke, but little is known about its mechanism. We investigated 10 consecutive patients with heatstroke (mean age 58 +/- 2 yr) whose mean rectal temperature at admission was 42.3 +/- 0.2 degrees C. Eight patients presented with hypophosphatemia [0.48 +/- 0.08 mmol/l, normal range (NR) 0.8–1.4 mmol/l], associated with increased fractional excretion of phosphate (19.8 +/- 6.4%, NR 6–20%) relative to plasma phosphate levels and reduced renal threshold for phosphate (0.55 +/- 0.08 mmol/l glomerular filtrate, NR 0.8–1.4 mmol/l). Plasma parathyroid hormone (75.0 +/- 5 pmol/l) and calcium (2.24 +/- 0.02 mmol/l) levels and fractional excretion of calcium were normal (1.66 +/- 0.27%). There was no evidence of uricosuria or aminoaciduria, and only one patient had glucosuria. Arterial carbon dioxide was decreased in eight patients (28 +/- 1.1 Torr); however, none had elevated blood pH (7.35 +/- 0.02). The results suggest that heatstroke-related hypophosphatemia is associated with abnormal phosphaturia independent of the parathyroid hormone level, and there is no evidence of tubular dysfunction.

Developmental changes in the phosphaturic response to parathyroid hormone in the rat

1985 ◽  
Vol 249 (2) ◽  
pp. F251-F255 ◽  
Author(s):  
S. K. Webster ◽  
A. Haramati
Keyword(s):  
Parathyroid Hormone ◽  
Fractional Excretion ◽  
Developmental Changes ◽  
High Dose ◽  
Kidney Weight ◽  
Phosphate Excretion ◽  
Immature Rats ◽  
Glomerular Filtrate ◽  
Old Rats ◽  
Fractional Excretion Of Phosphate

The need for young, immature rats to maintain positive phosphate balance for growth is well recognized. However, whether this process is associated with a resistance to the phosphaturic effect of parathyroid hormone (PTH) is not clear. In these experiments we examined the effect of PTH on urinary phosphate and cAMP excretion in rats at 3, 6, 12, and 20 wk of age. Clearance experiments were performed in acutely thyroparathyroidectomized (TPTX) rats fed a normal phosphate diet (0.86%). Basal fractional excretion of phosphate (FEPi) was low in all TPTX rats (less than 1%). The phosphaturic response to a high dose of PTH (1 U X kg-1 X min-1) increased with development (from 4 to 29%). The responses to increasing doses of PTH demonstrated a decrease in sensitivity to PTH in 6- compared with 20-wk-old rats. Urinary cAMP excretion (either per milliliter glomerular filtrate or per gram kidney weight) following PTH was not different among 6-, 12-, and 20-wk-old rats, thus demonstrating a dissociation between the increase in phosphate excretion and cAMP excretion. These results indicate that the phosphaturic response to PTH is blunted in immature, acutely TPTX rats and that the phosphaturia increases progressively with development.

Effect of dietary phosphate on transport properties of pig renal microvillus vesicles

1980 ◽  
Vol 239 (4) ◽  
pp. F352-F359 ◽  
Author(s):  
Paula Q. Barrett ◽  
Joseph M. Gertner ◽  
Howard Rasmussen
Keyword(s):  
Phosphate Uptake ◽  
Membrane Vesicle ◽  
Membrane Vesicles ◽  
Phosphate Transport ◽  
Transport Systems ◽  
Sodium Gradient ◽  
Microvillus Membrane ◽  
Dietary Phosphate ◽  
Dependent Transport ◽  
High Phosphate

Dietary phosphate manipulation results in stable adaptive changes in the transport functions of microvillus membrane vesicles isolated from pig renal cortex. When assayed under sodium gradient conditions, phosphate uptake is enhanced 200–400% in vesicles prepared from animals maintained on a low-phosphate diet (0.22%) compared to high-phosphate diet controls (0.82%). When transport is assayed in sodium preequilibrated vesicles, a 100% enhancement of phosphate uptake is demonstrable. Stimulation of phosphate uptake into low-phosphate diet vesicles after the imposition of a sodium chloride gradient is equivalent if uptake is measured at pH 6.0 or 8.0 and can be kinetically characterized as resulting from a Vmax alteration in the phosphate transport system. Microvillus membrane vesicle phosphate transport is maximally stimulated after only 2 days of dietary deprivation. Although a longer period (1 and 2 wk) of phosphate restriction does not further stimulate phosphate transport, it does result in an inhibition of other sodium gradient-dependent transport systems (glucose, alanine). phosphate transport; phosphate restriction; glucose transport; brush-border vesicles Submitted on October 22, 1979 Accepted on April 25, 1980

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