Phosphaturic effect of L-NMMA in the presence of parathyroid hormone

1996 ◽  
Vol 271 (6) ◽  
pp. R1477-R1480
Author(s):  
M. J. Onsgard-Meyer ◽  
R. J. Kerrigan ◽  
M. Collins ◽  
A. A. Khraibi ◽  
F. G. Knox
Keyword(s):  
Parathyroid Hormone ◽  
Fractional Excretion ◽  
Parathyroid Glands ◽  
Constant Infusion ◽  
Sprague Dawley ◽  
Phosphate Excretion ◽  
Sprague Dawley Rats ◽  
Additional Group ◽  
Renal Clearances ◽  
Intact Rats

The objective of this study was to examine the effect of NG-monomethyl-L-arginine (L-NMMA) on phosphate excretion in the presence and absence of parathyroid hormone (PTH). Renal clearances were obtained before and during infusion of L-NMMA (15 mg/kg bolus and 500 micrograms.kg-1.min-1 infusion) in Sprague-Dawley rats with intact parathyroid glands (n = 6), in thyroparathyroidectomized (TPTX) rats receiving a constant infusion of PTH-(1-34) (0.01-0.03 U.kg-1.min-1) (n = 11) throughout the experiment, or in TPTX rats, that received an acute infusion of PTH-(1-34) (33 U/kg bolus and 1 U.kg-1.min-1 infusion) after L-NMMA infusion alone (n = 7). In rats with intact parathyroid glands, L-NMMA increased the fractional excretions of phosphate (FEPi) and sodium (FENa) and mean arterial pressure (MAP) (delta 8.6 +/- 1.5%, delta 0.62 +/- 0.1%, and delta 26.7 +/- 4.9 mmHg, respectively; P < 0.05). In TPTX rats receiving a constant infusion of PTH, L-NMMA again increased FEPi, FENa, and MAP (delta 9.5 +/- 3.6%, delta 1.1 +/- 0.4%, and delta 28.4 +/- 4.5 mmHg, respectively; P < 0.05). However, in TPTX rats, L-NMMA alone did not increase FEPi (delta 0.9 +/- 0.3%), whereas the subsequent infusion of PTH with L-NMMA increased FEPi (delta 15.6 +/- 3.1%; P < 0.05). In an additional group of intact and TPTX rats, the fractional excretion of lithium (FELi) was measured as an index of proximal reabsorption. L-NMMA increased FELi in intact rats (delta 13.2 +/- 2.6%; P < 0.05), but not in TPTX rats (delta 4.2 +/- 3.3%). In conclusion, L-NMMA increases phosphate excretion in association with increases in MAP and FENa, and this phosphaturic effect is dependent on the presence of PTH.

scholarly journals Mechanism of dopamine inhibition of renal phosphate transport.

1992 ◽  
Vol 2 (11) ◽  
pp. 1601-1607
Author(s):  
J Isaac ◽  
R P Glahn ◽  
M M Appel ◽  
M Onsgard ◽  
T P Dousa ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Brush Border Membrane ◽  
Phosphate Transport ◽  
Constant Infusion ◽  
Saline Control ◽  
Control Group ◽  
Sprague Dawley ◽  
Pi Transport ◽  
Sprague Dawley Rats ◽  
Dependent Transport

Dopamine (DA) is natriuretic and phosphaturic. However, whether the effect of DA on Pi reabsorption is a consequence of its effect on sodium transport is not known. Therefore, this study was performed to determine the effect of DA on the maximal transport of phosphate (TmPi), and upon the capacity of renal proximal brush border membrane (BBM) for (Naextra-vesicular greater than Naintravesicular)-gradient-dependent transport of Pi, as compared with the transport of other solutes. Graded infusions of Pi (0, 1, 2, and 3 mumols/min) were given to thyroparathyroidectomized male Sprague-Dawley rats in the presence of vehicle (0.9% NaCl; N = 5), DA 15 micrograms/kg/min; N = 6), or parathyroid hormone ((PTH); 1 U/kg/min; N = 5). The TmPi for rats infused with DA (3.3 +/- 0.3 mumol/mL) was significantly less than the TmPi for saline control rats (4.4 +/- 0.2 mumol/mL). Rats infused with PTH exhibited the lowest TmPi (1.8 +/- 0.3 mumol/mL). No differences in sodium excretion were observed among any of the groups. Na-dependent Pi transport was studied in BBM vesicles (BBMV) prepared from rats fed a low-phosphate diet for 2 days that were anesthetized, acutely thyroparathyroidectomized, and systemically infused with DA (350 micrograms bolus, plus 35 micrograms/kg/min; N = 8), PTH (33 U/kg bolus, followed by a continuous infusion of 1 U/kg/min; N = 6), or vehicle (1 mL/kg bolus, plus 2 mL/h constant infusion of 0.9% NaCl; N = 8) for 90 min. DA significantly inhibited the Na cotransport of Pi by 22.4 +/- 4.1% (P less than 0.01) as compared with the control group.(ABSTRACT TRUNCATED AT 250 WORDS)

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)

Parathyroid hormone contributes to volume expansion-induced inhibition of proximal reabsorption

1985 ◽  
Vol 248 (1) ◽  
pp. F100-F103 ◽  
Author(s):  
O. Mercier ◽  
M. Bichara ◽  
M. Paillard ◽  
J. P. Gardin ◽  
F. Leviel
Keyword(s):  
Parathyroid Hormone ◽  
Volume Expansion ◽  
Sprague Dawley ◽  
Nacl Transport ◽  
Free Expansion ◽  
Group Iii ◽  
Group I ◽  
Sprague Dawley Rats ◽  
Stimulation Of ◽  
Intact Rats

Volume expansion inhibits the proximal reabsorption of water, bicarbonate, and chloride. The present work tested a hypothetical role of parathyroid hormone (PTH) in the expansion effect. We studied 19 Sprague-Dawley rats during a plasma-replete euvolemic state and following 10% body wt colloid-free expansion. In group I, six intact rats, volume expansion decreased plasma ionized calcium concentration ([Ca2+]P) from 2.28 +/- 0.06 to 2.11 +/- 0.04 meq/liter and increased nephrogenous cAMP (NcAMP) from 29 +/- 5 to 66 +/- 10 pmol X min-1 X g kidney wt-1. In group II, six acutely thyroparathyroidectomized (TPTX) rats, [Ca2+]P also fell from 2.18 +/- 0.08 to 1.80 +/- 0.08 meq/liter but NcAMP did not rise significantly (9 +/- 3 vs. 17 +/- 5 pmol X min-1 X g kidney wt-1). These data strongly suggest that stimulation of PTH activity occurred during expansion in intact animals. In group III, seven TPTX rats, volume expansion inhibited proximal reabsorption of total CO2 by 11%, of chloride by 24%, and of water by 19%. Volume expansion-induced reduction in bicarbonate, chloride, and water reabsorption was smaller in TPTX than in intact rats previously studied. We conclude that volume expansion inhibits proximal reabsorption in part by decreasing the active transcellular NaHCO3 and NaCl transport secondary to stimulation of PTH activity.

Parathyroïdes et hypertension artérielle à l'acétate de désoxycorticostérone chez le rat

1979 ◽  
Vol 57 (2) ◽  
pp. 157-162 ◽  
Author(s):  
A. Berthelot ◽  
R. Schleiffer ◽  
A. Gairard
Keyword(s):  
Blood Pressure ◽  
Parathyroid Hormone ◽  
Arterial Hypertension ◽  
Mechanism Of Action ◽  
Parathyroid Glands ◽  
Sprague Dawley ◽  
Deoxycorticosterone Acetate ◽  
Hypertension Artérielle ◽  
Sprague Dawley Rats

We studied the importance of parathyroids in the development of mineralocorticoid hypertension in male Sprague–Dawley rats. Ablation of the parathyroids 1 week before deoxycorticosterone acetate (DOCA) + NaCl administration prevented development of hypertension (for 1 year). But ablation of parathyroids 2 weeks after the start of treatment has no effect on the development of arterial hypertension. Autotransplantation of parathyroids in thyroidectomized rats caused a recurrence of mineralocorticoid hypertension, which was completed after DL-thyroxine supplementation: blood pressure levels were nearly the same as in DOCA sham rats. We conclude that parathyroid glands favor the establishment of mineralocorticoid hypertension in the rat. These results raise the question of the mechanism of action of parathyroid hormone in the hypertensive process.

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)

Parathyroid Hormone- and Deoxycorticosterone Acetate-Induced Hypertension in the Rat

1980 ◽  
Vol 58 (5) ◽  
pp. 365-371 ◽  
Author(s):  
A. Berthelot ◽  
A. Gairard
Keyword(s):  
Parathyroid Hormone ◽  
Hormone Secretion ◽  
Sprague Dawley ◽  
Physiological Concentration ◽  
Deoxycorticosterone Acetate ◽  
Calcium Diet ◽  
Arterial Blood ◽  
Sprague Dawley Rats ◽  
High Calcium ◽  
High Calcium Diet

1. Hypertension induced by treatment with deoxycorticosterone acetate and sodium chloride was studied in male Sprague-Dawley rats and related to parathyroid hormone secretion. 2. Lack of parathyroid hormone (due to parathyroidectomy) or decreased parathormone secretion (due to a high-calcium diet) partially inhibited the development of arterial hypertension. 3. In contrast, in thyroparathyroidectomized rats supplemented with thyroxine, the administration of parathyroid hormone rapidly elevated arterial blood pressure. 4. Maintaining a physiological concentration of serum calcium in the absence of parathyroid hormone (by feeding a high-calcium diet to parathyroidectomized rats) was not sufficient to establish mineralocorticoid hypertension. 5. These results show that parathyroid hormone is necessary for the complete development of mineralocorticoid hypertension.

scholarly journals Renal haemodynamic and tubular actions of urotensin II in the rat

2008 ◽  
Vol 198 (3) ◽  
pp. 617-624 ◽  
Author(s):  
Alaa E S Abdel-Razik ◽  
Ellen J Forty ◽  
Richard J Balment ◽  
Nick Ashton
Keyword(s):  
Body Weight ◽  
Renal Medulla ◽  
Fractional Excretion ◽  
Haemodynamic Effects ◽  
Urotensin Ii ◽  
Sprague Dawley ◽  
Minimal Impact ◽  
Sprague Dawley Rats ◽  
Fractional Excretion Of Sodium ◽  
Excretion Rates

Urotensin II (UTS) is a potent vasoactive peptide that was originally identified in teleost fish. Mammalian orthologues of UTS and its receptor (UTSR) have been described in several species, including humans and rats. We have shown previously that bolus injections of UTS caused a decrease in urine flow and sodium excretion rates in parallel with marked reductions in renal blood flow (RBF) and glomerular filtration rate (GFR). The aim of this study was to determine the effect of UTS infusion at a dose that has minimal impact upon renal haemodynamics in order to identify a potential direct tubular action of UTS. Infusion of rat UTS (rUTS) at 0.6 pmol/min per 100 g body weight in male Sprague–Dawley rats, which had no effect on RBF and caused a 30% reduction in GFR, resulted in a significant increase in the fractional excretion of sodium (vehicle 2.3±0.6 versus rUTS 0.6 pmol 4.5±0.6%, P<0.05) and potassium. At the higher dose of 6 pmol/min per 100 g body weight, haemodynamic effects dominated the response. rUTS induced a marked reduction in RBF and GFR (vehicle 1.03±0.06 versus rUTS 6 pmol 0.31±0.05 ml/min per 100 g body weight, P<0.05) resulting in an anti-diuresis and anti-natriuresis, but no change in fractional excretion of sodium or potassium. Uts2d and Uts2r mRNA expression were greater in the renal medulla compared with the cortex. Together, these data support an inhibitory action of Uts2d on renal tubule sodium and potassium reabsorption in the rat, in addition to its previously described renal haemodynamic effects.

Rapid determination of glomerular filtration rate by single-bolus inulin: a comparison of estimation analyses

1998 ◽  
Vol 84 (6) ◽  
pp. 2154-2162 ◽  
Author(s):  
Cord Sturgeon ◽  
Albert D. Sam ◽  
William R. Law
Keyword(s):  
Mathematical Model ◽  
Glomerular Filtration Rate ◽  
Mathematical Models ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Rapid Determination ◽  
Constant Infusion ◽  
Sprague Dawley ◽  
Single Bolus ◽  
Sprague Dawley Rats

Rapid measurement of glomerular filtration rate (GFR) by an inulin single-bolus technique would be useful, but its accuracy has been questioned. We hypothesized that reported inaccuracies reflect the use of inappropriate mathematical models. GFR was measured in 14 intact and 5 unilaterally nephrectomized conscious male Sprague-Dawley rats (mean weight 368 ± 12 g) by both single-bolus (25 mg/kg) and constant-infusion techniques (0.693 mg ⋅ kg−1 ⋅ min−1). The temporal decline in plasma inulin concentration was analyzed through biexponential curve fitting, which accounted for renal inulin loss before complete vascular and interstitial mixing. We compared our mathematical model based on empirical rationale with those of other investigators whose studies suggest inaccuracy of single-bolus methods. Our mathematical model yielded GFR values by single bolus that agreed with those obtained by constant infusion [slope = 0.94 ± 0.16 (SE); y intercept = 0.23 ± 0.64; r = 0.82]. In comparison to the data obtained by constant inulin infusion, this method yielded a very small bias of −0.0041 ± 0.19 ml/min. Two previously reported models yielded unsatisfactory values (slope = 1.46 ± 0.34, y intercept = 0.47 ± 1.5, r = 0.72; and slope = 0.17 ± 1.26, y intercept = 17.15 ± 5.14, r = 0.03). The biases obtained by using these methods were −2.21 ± 0.42 and −13.90 ± 1.44 ml/min, respectively. The data indicate that when appropriate mathematical models are used, inulin clearance after single-bolus delivery can be used to measure GFR equivalent to that obtained by constant infusion of inulin. Attempts to use methods of analysis for simplicity or expediency can result in unacceptable measurements relative to the clinical range of values seen.

scholarly journals Interaction between serum FGF-23 and PTH in renal phosphate excretion, a case-control study in hypoparathyroid patients

2019 ◽  
Author(s):  
Forough Saki ◽  
Seyed Reza Kassaee ◽  
Azita Salehifar Salehifar ◽  
gholamhossein Ranjbar omrani
Keyword(s):  
Parathyroid Hormone ◽  
Serum Calcium ◽  
Case Control Study ◽  
Fractional Excretion ◽  
Case Control ◽  
Control Group ◽  
Phosphate Excretion ◽  
Significant Difference ◽  
Fgf 23 ◽  
Control Study

Abstract Background:phosphate homeostasis is mediated through complex counter regulatory feed-back balance between parathyroid hormone, FGF-23 and 1,25(OH)2D. Both parathyroid hormone and FGF-23 regulate proximal tubular phosphate excretion through signaling on sodium- phosphate cotransporters II a and II c . However, the interaction between these hormones on phosphate excretion is not clearly understood. We performed the present study to evaluate whether the existence of sufficient parathyroid hormone is necessary for full phosphaturic function of FGF-23 or not. Methods:In this case-control study, 19 patients with hypoparathyroidism and their age- and gender-matched normal population were enrolled. Serum calcium, phosphate, alkaline phosphatase,parathyroid hormone, FGF-23, 25(OH)D, 1,25(OH)2D and Fractional excretion of phosphorous were assessed and compared between the two groups, using SPSS software. Results:The mean serum calcium and parathyroid hormone level was significantly lower in hypoparathyroid patients in comparison with the control group(P<0.001 and P<0.001, respectively). We found high serum level of phosphate and FGF-23 in hypoparathyroid patients compared to the control group (P<0.001 and P<0.001,respectively). However, there was no significant difference in Fractional excretion of phosphorous or 1,25OH2D level between the two groups. There was a positive correlation between serum FGF-23 and Fractional excretion of phosphorous just in the normal individuals (P <0.001, r = 0.79). Conclusions:Although the FGF-23 is a main regulator of urinary phosphate excretion but the existence of sufficient parathyroid hormone is necessary for the full phosphaturic effect of FGF-23.

Lithium administration and phosphate excretion

1976 ◽  
Vol 231 (4) ◽  
pp. 1140-1146 ◽  
Author(s):  
JA Arruda ◽  
JM Richardson ◽  
JA Wolfson ◽  
L Nascimento ◽  
DR Rademacher ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Cyclic Amp ◽  
Renal Cortex ◽  
Cyclic Adenosine Monophosphate ◽  
Fractional Excretion ◽  
Adenosine Monophosphate ◽  
Adenyl Cyclase ◽  
Phosphate Excretion ◽  
Camp System

The phosphaturic effect of parathyroid hormone (PTH), cyclic adenosine monophosphate (cAMP), acetazolamide (Az), and HCO3 loading was studied in normal, thyroparathyroidectomized (TPTX), and Li-treated dogs. PTH administration to normal animals markedly increased fractional excretion (F) of PO4 but had a blunted effect on FPO4 in the Li-treated animals. Cyclic AMP likewise markedly increased FPO4 in the normal animals but had a markedly blunted effect in the Li-treated animals. Az led to a significant increase in FNa, FHCO3, and FPO4 in the normal animals. In the Li-treated dogs, Az induced a significant natriuresis and bicarbonaturia but failed to increase phosphaturia. HCO3 loading in normal dogs caused a significant phosphaturia while having little effect on FPO4 in Li-treated dogs. HCO3 loading to TPTX dogs was associated with a lower FPO4 as compared to normal HCO3-loaded animals. These data suggest that Li administration not only blocks the adenyl cyclase-cAMP system in the renal cortex, but it may also interfere with a step distal to the formation of cAMP, since the phosphaturic effect of both PTH and cAMP was markedly diminished in Li-treated animals.

Sign in / Sign up

Export Citation Format

Share Document