Effect of acute hypoxia on phosphate excretion in rats

1994 ◽  
Vol 266 (2) ◽  
pp. R578-R583
Author(s):  
Y. Mimura ◽  
F. G. Knox
Keyword(s):  
Acute Hypoxia ◽  
Fractional Excretion ◽  
Respiratory Alkalosis ◽  
Renal Handling ◽  
Arterial Pco2 ◽  
Phosphate Excretion ◽  
Fractional Excretion Of Phosphate ◽  
Spontaneously Breathing ◽  
Arterial Po2 ◽  
Hypoxic Group

This study evaluated the effect of acute hypoxia on renal handling of phosphate in rats in the presence and absence of parathyroid hormone (PTH). Hypoxia causes respiratory alkalosis in spontaneously breathing humans and animals. Respiratory alkalosis has been reported to induce a blunted phosphaturic response to PTH. In this study, to avoid the confounding effect of hypocapnia accompanying the hypoxia on phosphate excretion, the rats were ventilated mechanically, and arterial PCO2 levels were controlled. Rats were divided into two main groups depending on the arterial PO2 levels: a hypoxic group (n = 16) and a normoxic group (n = 18). Hypoxia was produced by ventilating with 10% oxygen, and hypocapnia was produced by hyperventilation. In response to PTH, the hypoxic rats without hypocapnia showed a greater increase in fractional excretion of phosphate (FEPi; 37.7 +/- 2.6%, mean +/- SE) compared with normoxic rats (27.4 +/- 2.5%, P < 0.02). During hypocapnia, there was no difference in FEPi between hypoxic and normoxic groups (21.2 +/- 1.5 and 19.5 +/- 1.2%, respectively), and both groups showed a significantly blunted phosphaturic response to PTH compared with normocapnia (P < 0.05 and P < 0.01, respectively). Urinary adenosine 3',5'-cyclic monophosphate (cAMP) increased similarly after PTH infusion between each group. To test whether the phosphaturic effect of PTH in hypoxia and the blunted phosphaturic effect of PTH in hypocapnia are due to steps beyond the generation of cAMP, the phosphaturic response to cAMP infusion was evaluated in 1) hypoxic and normocapnic rats (n = 6), 2) normoxic and normocapnic (control) rats (n = 6), and 3) normoxic and hypocapnic rats (n = 7).(ABSTRACT TRUNCATED AT 250 WORDS)

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) (&gt; 0.58) were matched by age and sex to participants with a low risk WHtR (&lt;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&lt;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&lt;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.

Effect of hypoxia on metabolic rate in awake ponies

1994 ◽  
Vol 76 (6) ◽  
pp. 2380-2385 ◽  
Author(s):  
M. J. Korducki ◽  
H. V. Forster ◽  
T. F. Lowry ◽  
M. M. Forster
Keyword(s):  
Metabolic Rate ◽  
Chronic Hypoxia ◽  
Acute Hypoxia ◽  
Pulmonary Ventilation ◽  
Time Dependent ◽  
Hypoxic Hypoxia ◽  
Arterial Pco2 ◽  
Breathing Room ◽  
Arterial Po2 ◽  
Transient Failure

To determine the effect of hypoxia on metabolic rate (VO2) of ponies, on 2 days we studied ponies that were breathing room air for 1 h followed by 5 h of either hypoxic hypoxia (fractional concn of inspired O2 = 0.126) or 5 h of CO hypoxia. Control arterial PO2 was 103 +/- 1.2 Torr, and at 5 min and 5 h of hypoxic hypoxia, arterial PO2 was 53.1 +/- 1.8 and 41.0 +/- 1.8 Torr, respectively. There was a time-dependent hypocapnia and alkalosis during hypoxic hypoxia. During CO hypoxia, carboxyhemoglobin increased to 25% after 30 min and remained constant thereafter. With increased carboxyhemoglobin, arterial PCO2 was 1.3 Torr above (P < 0.05) and 1.5 Torr (P < 0.05) below control levels after 30 min and 3 h, respectively. There were no significant (P > 0.10) changes in VO2 during either hypoxic or CO hypoxia. However, in 50% of the ponies, VO2, pulmonary ventilation, and rectal temperature increased and shivering was evident after 30 min of hypoxia. Peak values of pulmonary ventilation, VO2, and shivering occurred at approximately 2 h with a subsequent return toward control levels. We conclude that, in contrast to smaller mammals, acute hypoxia does not depress VO2 of ponies. The hypermetabolism and hyperthermia during chronic hypoxia in some ponies may reflect a transient failure in thermoregulation.

scholarly journals Acute hypoxia and endogenous renal endothelin.

1994 ◽  
Vol 4 (11) ◽  
pp. 1920-1924
Author(s):  
A Nir ◽  
A L Clavell ◽  
D Heublein ◽  
L L Aarhus ◽  
J C Burnett
Keyword(s):  
Acute Hypoxia ◽  
Fractional Excretion ◽  
Urinary Sodium Excretion ◽  
Renal Tissue ◽  
Control Group ◽  
Moderate Hypoxia ◽  
Time Control ◽  
Fractional Excretion Of Sodium ◽  
Air Ventilation ◽  
Hypoxic Group

Endothelin (ET) is a potent vasoconstrictor peptide of endothelial cell origin. Recent studies have suggested a nonvascular paracrine and/or autocrine role for endothelin in the kidney. This study was designed to elucidate the renal ET response to acute moderate hypoxia, as reflected by urinary ET excretory rate and renal tissue ET immunoreactivity, and to correlate these responses to the hemodynamic and excretory changes during hypoxia. Experiments were conducted in two groups of anesthetized dogs: hypoxic group (10% O2 ventilation: PO2, 44 mm Hg; N = 7) and time control group (room air ventilation: PO2, 111 mm Hg; N = 6). After 60 min of hypoxia or room air ventilation, kidneys were harvested and stained immunohistochemically for ET. Acute moderate hypoxia was associated with significant increases in urinary ET excretion, urine flow, urinary sodium excretion, and fractional excretion of sodium (P < 0.05). There was no significant change in GFR, RBF, renal vascular resistance, or mean arterial pressure. Renal immunohistochemistry for ET revealed increased staining in the proximal and distal tubules in the hypoxic group as compared with controls. This study demonstrates that acute moderate hypoxia results in increased urinary ET excretion and renal tubular ET immunoreactivity, in association with diuresis and natriuresis, and suggests a nonvascular role of endogenously produced renal ET in the regulation of sodium homeostasis during hypoxia.

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)

Effect of aluminum on the renal handling of phosphate in the rat

1985 ◽  
Vol 248 (1) ◽  
pp. F64-F69
Author(s):  
M. Burnatowska-Hledin ◽  
A. M. Klein ◽  
G. H. Mayor
Keyword(s):  
Filtration Rate ◽  
Control Period ◽  
Fractional Excretion ◽  
Plasma Calcium ◽  
Urine Flow ◽  
Plasma Sodium ◽  
Renal Handling ◽  
Blood Ph ◽  
Fractional Excretion Of Phosphate ◽  
To Receive

The effects of aluminum (Al) on the renal handling of phosphate (Pi) were studied by clearance techniques in the presence and absence of endogenous parathyroid hormone (PTH) and after Pi infusion. In all groups, a 1-h control period was followed by three 1-h experimental periods in which controls continued to receive saline and experimental animals received Al. Glomerular filtration rate, urine flow rate, and plasma sodium (Na) were not significantly changed between periods in any group. In the presence of endogenous PTH, the fractional excretion of phosphate (FEPi) increased significantly after 3 h of Al infusion (6.1 +/- 0.9 to 15.0 +/- 1.8%, P less than 0.05, n = 8), but not in controls (n = 7), while plasma calcium and Pi decreased, suggesting a PTH effect. However, in acutely thyroparathyroidectomized (TPTX) rats the FEPi also increased significantly after 3 h of Al infusion (4.3 +/- 3.0 to 10.6 +/- 4.2%, P less than 0.05, n = 7), but not in controls (n = 6). In TPTX rats infused with Pi where plasma Pi was increased to 10 mg/dl, FEPi increased significantly after 2 and 3 h of Al (7.0 +/- 1.4 to 15.5 +/- 2.1 to 16.9 +/- 2.2%, P less than 0.01, n = 15), but not in controls (n = 8). In this group, changes in FEPi were accompanied by a small but significant increase in FENa but not urinary cAMP. Blood pH was not significantly different between saline and Al-infused rats. These studies indicate that Al infusion inhibits renal Pi reabsorption by a mechanism independent of PTH, blood pH, or cAMP.

Renal handling of phosphate during acute respiratory acidosis and alkalosis in the rat

1984 ◽  
Vol 247 (4) ◽  
pp. F596-F601 ◽  
Author(s):  
A. Haramati ◽  
D. Nienhuis
Keyword(s):  
Carbon Dioxide ◽  
Respiratory Acidosis ◽  
Fractional Excretion ◽  
Transport Capacity ◽  
Plasma Phosphate ◽  
Acid Base ◽  
Renal Handling ◽  
Phosphate Reabsorption ◽  
Intrinsic Capacity ◽  
Fractional Excretion Of Phosphate

Clearance experiments were performed in acutely thyroparathyroidectomized rats to evaluate the renal handling of phosphate during respiratory acidosis (R ACID) and alkalosis (R ALK) in rats fed either a normal (0.7%) or low (0.07%) phosphate diet for 4 days. Different acid-base states were achieved by varying the mixture of carbon dioxide in the inspired air. Each group received graded infusions of phosphate to control for differences in plasma phosphate (PPi) and to determine the maximum transport capacity of phosphate reabsorption (TmPi/GFR). In rats fed a normal phosphate diet, PPi and the fractional excretion of phosphate (FEPi) were significantly greater in R ACID than in R ALK. However, there were no differences between R ACID and R ALK when FEPi was evaluated as a function of the PPi, and values for TmPi/GFR during R ACID were not different from those during R ALK. In rats fed low phosphate diet, PPi during R ACID was significantly greater than during R ALK, yet FEPi was less than 1% in all groups due to an adaptive increase in TmPi/GFR. Further, the TmPi/GFR was similar irrespective of the acid-base state. We conclude that acute respiratory acid-base changes do not alter the intrinsic capacity of the kidney to reabsorb phosphate.

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.

Ventral medullary extracellular fluid pH and PCO2 during hypoxemia

1987 ◽  
Vol 63 (4) ◽  
pp. 1567-1571 ◽  
Author(s):  
S. Javaheri ◽  
L. J. Teppema
Keyword(s):  
Steady State ◽  
Extracellular Fluid ◽  
Acid Base ◽  
Arterial Pco2 ◽  
Mean Values ◽  
Designed Experiments ◽  
Ventilatory Depression ◽  
Spontaneously Breathing ◽  
Arterial Po2 ◽  
Made In

We designed experiments to study changes in ventral medullary extracellular fluid (ECF) PCO2 and pH during hypoxemia. Measurements were made in chloralose-urethan-anesthetized spontaneously breathing cats (n = 12) with peripherial chemodenervation. Steady-state measurements were made during normoxemia [arterial PO2 (PaO2) = 106 Torr], hypoxemia (PaO2 = 46 Torr), and recovery (PaO2 = 105 Torr), with relatively constant arterial PCO2 (approximately 44 Torr). Mean values of ventilation were 945, 683, and 1,037 ml/min during normoxemia, hypoxemia, and recovery from hypoxemia, respectively. Ventilatory depression occurred in each cat during hypoxemia. Mean values of medullary ECF PCO2 were 57.7 +/- 7.2 (SD), 59.4 +/- 9.7, and 57.4 +/- 7.2 Torr during normoxemia, hypoxemia, and recovery to normoxemia, respectively; respective values for ECF [H+] were 60.9 +/- 8.0, 64.4 +/- 11.6, and 62.9 +/- 9.2 neq/l. Mean values of calculated ECF [HCO3-] were 22.8 +/- 3.0, 21.7 +/- 3.3, and 21.4 +/- 3.1 meq/l during normoxemia, hypoxemia, and recovery, respectively. Changes in medullary ECF PCO2 and [H+] were not statistically significant. Therefore hypoxemia caused ventilatory depression independent of changes in ECF acid-base variables. Furthermore, on return to normoxemia, ventilation rose considerably, still independent of changes in ECF PCO2, [H+], and [HCO3-].

ACTH secretion and ventilation increase at similar arterial PO2 in conscious rats

1989 ◽  
Vol 66 (5) ◽  
pp. 2245-2250 ◽  
Author(s):  
L. Jacobson ◽  
M. F. Dallman
Keyword(s):  
Acute Hypoxia ◽  
Exposure Period ◽  
Plasma Corticosterone ◽  
Acth Secretion ◽  
Arterial Pco2 ◽  
System Activity ◽  
Conscious Rats ◽  
Arterial Ph ◽  
Arterial Po2 ◽  
Adrenocortical System

To compare the arterial PO2 (PaO2) at which adrenocorticotropic hormone (ACTH) secretion and ventilation are stimulated, conscious rats with chronic femoral arterial catheters were exposed for 50 min to 21, 18, 15, 12, or 9% O2. Decreases in arterial PCO2 (PaCO2) and increases in arterial pH and adrenocortical system activity occurred consistently throughout the exposure period in rats exposed to 9 or 12% O2. In contrast, changes in PaCO2 or pH were only transient or delayed, plasma ACTH did not change, and plasma corticosterone only increased after 20 min in rats exposed to 15 or 18% O2 relative to those breathing 21% O2. Omitting the large blood sample at 20 min for ACTH eliminated the increase in corticosterone in the 15% O2 group. Overall, ACTH increased, and PaCO2 decreased, below PaO2 of approximately 60 Torr. We conclude that ACTH secretion increases at a similar PaO2 as hyperventilation-induced decreases in PaCO2 and thus represents a primary physiological response to acute hypoxia; hemodynamic stimuli may also interact with hypoxia to augment adrenocortical system activity.

Nephron site of resistance to phosphaturic effect of PTH during respiratory alkalosis

1985 ◽  
Vol 249 (6) ◽  
pp. F919-F922 ◽  
Author(s):  
T. J. Berndt ◽  
F. G. Knox
Keyword(s):  
Parathyroid Hormone ◽  
Proximal Tubule ◽  
Distal Tubule ◽  
Fractional Excretion ◽  
Respiratory Alkalosis ◽  
Proximal Convoluted Tubule ◽  
Phosphate Reabsorption ◽  
Hormone Administration ◽  
Pars Recta ◽  
Fractional Excretion Of Phosphate

This study was performed to evaluate the nephron site(s) responsible for the blunted phosphaturic effect of parathyroid hormone during respiratory alkalosis. In normocapnic thyroparathyroidectomized rats, parathyroid hormone administration markedly increased the fractional excretion of phosphate (FEp) from 2.1 +/- 0.5 to 36.6 +/- 5.0%. However, in the respiratory alkalotic rats, parathyroid hormone administration did not significantly increase the FEp (1.4 +/- 0.9 to 5.9 +/- 2.2%). This blunted phosphaturic response to parathyroid hormone was not due to a blunted inhibition of phosphate reabsorption by the superficial proximal tubule, since parathyroid hormone administration significantly increased the fractional delivery of phosphate (FDp) at the superficial late proximal tubule in both normal (25.3 +/- 3.0 to 36.2 +/- 3.8%, delta 10.9 +/- 3.2%) and respiratory alkalotic rats (12.2 +/- 3.1 to 30.3 +/- 4.9%, delta 18.0 +/- 4.7%). Parathyroid hormone administration significantly increased the FDp at the superficial early distal tubule from 9.3 +/- 3.9 to 38.7 +/- 7.4% (delta 29.4 +/- 5.1%) in normal rats and from 4.5 +/- 1.7 to 12.9 +/- 3.4% (delta 8.5 +/- 3.2%) in the respiratory alkalotic rats. We conclude that the blunted phosphaturic response to parathyroid hormone in respiratory alkalotic rats is not due to a blunted inhibition of phosphate reabsorption by the proximal convoluted tubule but is primarily due to enhanced reabsorption by the pars recta segment of the proximal tubule.

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