Plasma parathyroid hormone and divalent cation response to induction of acute metabolic acidosis

1982 ◽  
Vol 60 (12) ◽  
pp. 1505-1513 ◽  
Author(s):  
James R. Oster ◽  
Guido O. Perez ◽  
Janet M. Canterbury ◽  
Helen C. Alpert ◽  
Carlos A. Vaamonde
Keyword(s):  
Lactic Acid ◽  
Parathyroid Hormone ◽  
Metabolic Acidosis ◽  
Methylmalonic Acid ◽  
Magnesium Concentration ◽  
Acute Administration ◽  
Anesthetized Dogs ◽  
Acute Metabolic Acidosis ◽  
Plasma Magnesium ◽  
Cation Response

Since the effect of acute administration of acid upon blood magnesium and parathyroid hormone (PTH) is unclear we infused anesthetized dogs with saline (controls), HCl, lactic, and methylmalonic acids for 3 h. In all groups but lactic acid, plasma magnesium decreased; ionized calcium levels were increased by all three acids. Nevertheless, PTH increased in each of six dogs following methylmalonic acid and decreased in four of six animals after lactic acid. The decrease in plasma magnesium concentration after methylmalonic acid appeared to be an important factor in explaining the disparate PTH changes in these two groups because concomitant magnesium administration obviated the increases in PTH in four of six additional methylmalonic acid-infused dogs.

Secondary Citrullinemia with Hyperammonemia in Four Neonatal Cases of Pyruvate Carboxylase Deficiency

PEDIATRICS ◽  
1981 ◽  
Vol 68 (6) ◽  
pp. 914-914 ◽  
Author(s):  
F. X. Coude ◽  
H. Ogier ◽  
C. Marsac ◽  
A. Munnich ◽  
C. Charpentier ◽  
...  
Keyword(s):  
Lactic Acid ◽  
Metabolic Acidosis ◽  
Pyruvate Carboxylase ◽  
Pyruvate Carboxylase Deficiency ◽  
Acute Metabolic Acidosis ◽  
Pyruvate Ratio

Numerous cases of pyruvate carboxylase (PC) deficiency have been reported since its first description in 1968.1 We had the opportunity to study four neonates with this disorder. All patients had similar clinical and biochemical findings. Symptoms started during the first day of life with acute metabolic acidosis and lethargy. Serum lactic acid was always high (10 to 20 mM) with a lactate-pyruvate ratio between 50 and 100. Serum βOH butyrate was normal or slightly elevated but the βOH butyrate-acetoacetate ratio was constantly less than 1.

scholarly journals Calcitriol and the parathyroid hormone-ionized calcium curve: a comparison of methodologic approaches.

1996 ◽  
Vol 7 (3) ◽  
pp. 497-505
Author(s):  
R Ouseph ◽  
J D Leiser ◽  
S M Moe
Keyword(s):  
Parathyroid Hormone ◽  
Metabolic Acidosis ◽  
Parathyroid Gland ◽  
Secretory Activity ◽  
Ionized Calcium ◽  
Set Point ◽  
Before And After ◽  
Acute Metabolic Acidosis ◽  
Analytical Approaches ◽  
Maximum Minimum

Investigations of the effects of calcitriol on the inverse sigmoidal relationship between parathyroid hormone (PTH) and ionized calcium (iCa) have yielded contradictory conclusions, possibly because of variations in experimental and analytical approaches. To clarify the existing literature, PTH-iCa curves were constructed by inducing hypo- and hypercalcemia through alterations in dialysate calcium concentration in eight hemodialysis patients with mild to moderate secondary hyperparathyroidism. The effects of low (metabolic acidosis) versus normal bicarbonate dialysis were compared before and after 4 wk of intravenous calcitriol, in a cross-over design. The PTH-iCa curves were primarily evaluated by using a four-parameter model. In addition, a variety of alternative published analytic approaches were examined and PTH-iCa curve slopes were further evaluated after normalization by (maximum - minimum PTH). The latter partially corrects for gland mass and cell-secretory capacity, and therefore yields a purer measure of the sensitivity of secretory activity to changes in iCa. The results of the study indicate that calcitriol decreased basal, maximal, and minimal PTH and non-normalized slope (all P < 0.05), but did not affect set point or normalized slope, independent of the specific analytic approach. Acute metabolic acidosis did not affect the PTH-iCa curve. Thus, intravenous calcitriol appears to decrease parathyroid gland functional mass, as reflected by decreases in maximal and minimal PTH levels, but does not affect the sensitivity of the parathyroid gland to changes in iCa, as set point and normalized slope were unaffected.

Effects of acute metabolic acidosis on parathyroid hormone action and calcium mobilization

1976 ◽  
Vol 230 (1) ◽  
pp. 127-131 ◽  
Author(s):  
N Beck ◽  
SK Webster
Keyword(s):  
Parathyroid Hormone ◽  
Metabolic Acidosis ◽  
Serum Calcium ◽  
Calcium Concentration ◽  
Tubular Reabsorption ◽  
Calcium Mobilization ◽  
Measurable Effect ◽  
Bilateral Nephrectomy ◽  
Serum Calcium Concentration ◽  
Acute Metabolic Acidosis

Mechanisms through which metabolic acidosis increases calcium mobilization have been investigated in thyroparathyroidectomized rats with induction of acute metabolic acidosis by infusing NH4C1 intravenously. Acute metabolic acidosis directly raised serum calcium concentration and augmented the effect of parathyroid hormone (PTH) to raise serum calcium concentration. The same effects of metabolic acidosis were observed in rats with surgically removed intestines and bilateral nephrectomy, suggesting that acute metabolic acidosis directly increases calcium mobilization from bone and augments the effect of PTH to mobilize calcium from bone. In the kidney, acidosis directly inhibited the tubular reabsorption of calcium, but augmented the effect of PTH to increase tubular reabsorption of calcium. Acidosis had no measurable effect on calcitonin action.

Role of acidosis-induced increases in calcium on PTH secretion in acute metabolic and respiratory acidosis in the dog

2004 ◽  
Vol 286 (5) ◽  
pp. E780-E785 ◽  
Author(s):  
Ignacio López ◽  
Escolástico Aguilera-Tejero ◽  
José Carlos Estepa ◽  
Mariano Rodríguez ◽  
Arnold J. Felsenfeld
Keyword(s):  
Parathyroid Hormone ◽  
Metabolic Acidosis ◽  
Specific Effect ◽  
Respiratory Acidosis ◽  
Normal Value ◽  
Baseline Values ◽  
Acute Metabolic Acidosis ◽  
Sufficient Magnitude ◽  
Edta Infusion

Recently, we showed that both acute metabolic acidosis and respiratory acidosis stimulate parathyroid hormone (PTH) secretion in the dog. To evaluate the specific effect of acidosis, ionized calcium (iCa) was clamped at a normal value. Because iCa values normally increase during acute acidosis, we now have studied the PTH response to acute metabolic and respiratory acidosis in dogs in which the iCa concentration was allowed to increase (nonclamped) compared with dogs with a normal iCa concentration (clamped). Five groups of dogs were studied: control, metabolic (clamped and nonclamped), and respiratory (clamped and nonclamped) acidosis. Metabolic (HCl infusion) and respiratory (hypoventilation) acidosis was progressively induced during 60 min. In the two clamped groups, iCa was maintained at a normal value with an EDTA infusion. Both metabolic and respiratory acidosis increased ( P < 0.05) iCa values in nonclamped groups. In metabolic acidosis, the increase in iCa was progressive and greater ( P < 0.05) than in respiratory acidosis, in which iCa increased by 0.04 mM and then remained constant despite further pH reductions. The increase in PTH values was greater ( P < 0.05) in clamped than in nonclamped groups (metabolic and respiratory acidosis). In the nonclamped metabolic acidosis group, PTH values first increased and then decreased from peak values when iCa increased by >0.1 mM. In the nonclamped respiratory acidosis group, PTH values exceeded ( P < 0.05) baseline values only after iCa values stopped increasing at a pH of 7.30. For the same increase in iCa in the nonclamped groups, PTH values increased more in metabolic acidosis. In conclusion, 1) both metabolic acidosis and respiratory acidosis stimulate PTH secretion; 2) the physiological increase in the iCa concentration during the induction of metabolic and respiratory acidosis reduces the magnitude of the PTH increase; 3) in metabolic acidosis, the increase in the iCa concentration can be of sufficient magnitude to reverse the increase in PTH values; and 4) for the same degree of acidosis-induced hypercalcemia, the increase in PTH values is greater in metabolic than in respiratory acidosis.

Changes in brain ECF pH during metabolic acidosis and alkalosis: a microelectrode study

1983 ◽  
Vol 55 (6) ◽  
pp. 1849-1853 ◽  
Author(s):  
S. Javaheri ◽  
A. De Hemptinne ◽  
B. Vanheel ◽  
I. Leusen
Keyword(s):  
Cerebrospinal Fluid ◽  
Metabolic Acidosis ◽  
Metabolic Alkalosis ◽  
Extracellular Fluid ◽  
Acid Base ◽  
Brain Extracellular Fluid ◽  
Group I ◽  
Venous Pco2 ◽  
Anesthetized Dogs ◽  
Acute Metabolic Acidosis

We used pH-sensitive double-barreled microelectrodes to measure brain extracellular fluid (ECF) pH in anesthetized dogs during isocapnic infusion acidosis (HCl) and alkalosis (Na2CO3) of 45-60 min duration. The diameter of the tips of these electrodes varied from less than 1 to 27 micron and were placed 5 mm below the surface of the parietal cortex. In group I (metabolic acidosis, n = 5) mean plasma and brain ECF pH fell significantly by 0.221 and 0.025, respectively, with changes in brain ECF pH being 11.3% of those noted in plasma. In group II (metabolic alkalosis, n = 5) mean plasma and brain ECF pH rose significantly by 0.170 and 0.049, respectively, with changes in brain ECF pH being 28.8% of those noted in plasma. Mean arterial and sagittal venous PCO2 and cisternal cerebrospinal fluid (CSF) acid-base variables did not change significantly during acid or base infusion. We conclude that during transients of isocapnic metabolic acid-base perturbations ionic gradients exist between brain ECF and CSF and that changes in brain ECF pH measured by microelectrodes follow the changes in plasma pH. These pH changes may play an important role in respiratory adaptations of acute metabolic acidosis and alkalosis.

THE INFLUENCE OF PLASMA MAGNESIUM CONCENTRATION ON PARATHYROID HORMONE SECRETION

1968 ◽  
Vol 42 (4) ◽  
pp. 529-534 ◽  
Author(s):  
R. M. BUCKLE ◽  
A. D. CARE ◽  
C. W. COOPER ◽  
H. J. GITELMAN
Keyword(s):  
Parathyroid Hormone ◽  
Parathyroid Gland ◽  
Whole Blood ◽  
Hormone Secretion ◽  
Magnesium Content ◽  
Magnesium Concentration ◽  
Specific Radioimmunoassay ◽  
Constant Rate ◽  
Gland Function ◽  
Plasma Magnesium

SUMMARY The influence of plasma magnesium concentration on parathyroid gland function has been evaluated by perfusion at a constant rate of an isolated parathyroid gland in five goats and one sheep with whole blood of varying magnesium content. The concentration of magnesium in fresh whole blood was adjusted either by dialysis or by the addition of magnesium chloride before the perfusion. In each experiment, the concentration of calcium was maintained constant or was slightly altered to oppose the possible influence of magnesium on the rate of release of parathyroid hormone. Parathyroid hormone concentration in parathyroid venous plasma was estimated by a specific radioimmunoassay. In each experimental animal we observed that the concentration of parathyroid hormone in the effluent plasma diminished when the concentration of magnesium was raised or increased when the concentration of magnesium was lowered. These observations demonstrate a specific influence of magnesium on the rate of release of parathyroid hormone.

ABOLITION OF MAGNESIUM-INDUCED HYPOCALCAEMIA BY ACUTE THYRO-PARATHYROIDECTOMY IN THE CAT

1970 ◽  
Vol 64 (1) ◽  
pp. 150-158 ◽  
Author(s):  
S. Pors Nielsen
Keyword(s):  
Sodium Chloride ◽  
Flow Rate ◽  
Magnesium Chloride ◽  
Calcium Concentration ◽  
Plasma Calcium ◽  
Magnesium Concentration ◽  
Isotonic Sodium Chloride ◽  
Plasma Calcium Concentration ◽  
High Concentrations ◽  
Plasma Magnesium

ABSTRACT Intravenous infusion of isotonic magnesium chloride into young cats with a resultant mean plasma magnesium concentration of 7.7 meq./100 g protein was followed by a significant lowering of the plasma calcium concentration in 90 minutes. The rate of decrease of plasma calcium is consistent with the hypothesis that calcitonin is released by magnesium in high concentrations. There was no decrease in the plasma calcium concentration in cats of the same weight thyroparathyroidectomized 60 min before an identical magnesium chloride infusion or an infusion of isotonic sodium chloride at the same flow rate. The hypercalciuric effect of magnesium could not account for the hypocalcaemic effect of magnesium. Plasma magnesium concentration during magnesium infusion into cats with an intact thyroid-parathyroid gland complex was slightly, but not significantly higher than in acutely thyroparathyroidectomized cats.

scholarly journals Low plasma magnesium concentration and future abdominal aortic calcifications in moderate chronic kidney disease

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Anique D. ter Braake ◽  
◽  
Larissa P. Govers ◽  
Mieke J. Peeters ◽  
Arjan D. van Zuilen ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Vascular Calcification ◽  
Disease Risk ◽  
Statistical Significance ◽  
Cardiovascular Disease Risk ◽  
Magnesium Concentration ◽  
X Ray ◽  
Abdominal Aortic ◽  
Plasma Magnesium

Abstract Background Higher plasma magnesium concentrations are associated with reduced cardiovascular disease risk in chronic kidney disease (CKD) patients. The importance of plasma magnesium concentration for vascular calcification in earlier stages of CKD remains underexplored. This study investigated whether plasma magnesium is a determinant for the presence and severity of vascular calcification in moderate CKD. Methods Retrospective analysis was performed using abdominal aortic calcification (AAC) scores in 280 patients with stage 3 and 4 CKD enrolled in the MASTERPLAN trial. Lateral abdominal X-ray was used to evaluate AAC. Plasma magnesium concentration were measured over time. A zero-inflated Poisson model determined the association between plasma magnesium concentration and AAC. Results 79 out of 280 patients did not have AAC, and in patients with AAC the median calcification score was 3.5 (interquartile range: 0.0–8.6). The mean plasma magnesium concentration was 0.76 ± 0.10 mmol/L at baseline. A 0.1 mmol/L higher plasma magnesium concentration was associated with lower AAC of 0.07 point (95% CI -0.28 – 0.14). A 0.1 mmol/L higher plasma magnesium lowered the odds of detecting any AAC by 30% (OR = 0.63; 95% CI 0.29–1.37). After 1 year and 4 years (at time of X-ray) of follow-up this association was attenuated (OR = 0.93; 95% CI 0.61–1.43 and 0.93; 95% CI 0.60–1.45, respectively). None of these associations reached statistical significance. Conclusions Plasma magnesium concentration at baseline is not associated with the risk for future AAC. Interventions increasing magnesium to avoid vascular calcification may have greatest potential in early CKD stages prior to onset of vascular calcification.

scholarly journals ACUTE METABOLIC ACIDOSIS: EFFECTS ON ARGININE IN VASOPRESSIN(AVP) RELEASE IN FETAL SHEEP

1984 ◽  
Vol 18 ◽  
pp. 137A-137A
Author(s):  
Daniel J Faucher ◽  
Tom Lowe ◽  
About Laptook ◽  
John C Porter ◽  
Charles R Rosenfeld
Keyword(s):  
Metabolic Acidosis ◽  
Fetal Sheep ◽  
Acute Metabolic Acidosis
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