Mechanism of lithium-induced hypercalciuria in rats.

1978 ◽  
Vol 234 (3) ◽  
pp. E294
Author(s):  
K Lau ◽  
S Goldfarb ◽  
M Grabie ◽  
Z S Agus ◽  
M Goldberg
Keyword(s):  
Renal Tubule ◽  
Chronic Administration ◽  
Deficient Diet ◽  
Vitamin D Metabolism ◽  
Adequate Diet ◽  
Clearance Studies ◽  
Hormone Effects ◽  
Calcium Reabsorption ◽  
And Control ◽  
Absorptive Hypercalciuria

Chronic administration of lithium salts is associated with hypercalciuria in the rat. To study the renal and extrarenal mechanisms of this phenomenon, we utilized balance and clearance techniques in rats pair-fed diets with or without Li2CO3 (0.5 meq/day per rat). Lithium induced hypercalcemia (mean +/- SE: 5.40 +/- 0.09 VS. 5.06 +/- 0.05 meq/liter) and hypercalciuria (Ca/creatinine = 0.28 +/- 0.04 vs. 0.13 +/- 0.03) only during feeding. When CaCO2 supplement to a calcium-deficient diet was abruptly withdrawn, hypercalciuria was abolished. However, polyuria and polydipsia persisted. No significant changes in serum phosphate, urine phosphate, sodium, pH, or citrate were observed. Chronic parathyroidectomy (PTX) also abolished this effect. During clearance studies, fasting excretion of calcium was similar between treated and control animals. Superimposed acute PTX resulted in comparable changes, hence arguing against primary changes in renal calcium reabsorption or changes in parathyroid hormone effects on the renal tubule. Thus, lithium produces absorptive hypercalciuria by a mechanism dependent on intact parathyroid glands and adequate diet calcium, but independent of urine sodium, phosphate, or pH. The active component of gut calcium transport may be involved, possibly via alterations of vitamin D metabolism.

Glucocorticoid effects on respiration and metabolism by rat liver homogenates

1962 ◽  
Vol 202 (2) ◽  
pp. 343-346 ◽  
Author(s):  
Dennis D. Goetsch ◽  
L. E. McDonald
Keyword(s):  
Lactic Acid ◽  
Oxygen Uptake ◽  
Rat Liver ◽  
Inorganic Phosphate ◽  
Chronic Administration ◽  
Glucocorticoid Treatment ◽  
Carbohydrate Utilization ◽  
Protein Levels ◽  
Liver Homogenates ◽  
And Control

The effects of glucocorticoid administration on oxygen uptake, glucose and glycogen disappearance, lactic acid formation, and inorganic phosphate and protein levels in rat liver homogenates have been studied. A single injection of hydrocortisone, prednisolone, or 9 α-fluoroprednisolone 5 hr before sacrifice resulted in a highly significant increase in oxygen uptake by rat liver homogenates, whereas chronic administration of prednisolone daily for 7 days caused a marked inhibition in homogenate respiration. Glycolytic rate did not appear to be affected by single injections since endogenous carbohydrate utilization was similar in liver homogenates prepared from control and treated animals. Incubation of liver homogenates under aerobic conditions disclosed that inorganic phosphate levels were decreased in homogenates from corticoid-treated rats, whereas these levels were similar in treated and control liver homogenates incubated under nitrogen. Under anaerobic conditions, liver homogenates from treated rats accumulated lactic acid more rapidly than untreated liver homogenates. Glucocorticoid treatment did not appear to affect protein disappearance since no differences between protein levels in treated and untreated rat liver homogenates were detected following incubation.

Natriuresis in Rats Acutely Depleted of Chloride

1977 ◽  
Vol 52 (1) ◽  
pp. 23-31
Author(s):  
R. G. Luke ◽  
B. T. Khanh ◽  
R. D. Schmidt ◽  
J. H. Galla
Keyword(s):  
Sodium Bicarbonate Solution ◽  
Free Water ◽  
Sodium Reabsorption ◽  
Urinary Flow ◽  
Variable Degree ◽  
Water Reabsorption ◽  
Chloride Depletion ◽  
Sodium Load ◽  
Clearance Studies ◽  
And Control

1. Acute chloride depletion, without sodium depletion, was produced in rats by a single exchange peritoneal dialysis against sodium bicarbonate solution. Blood volume was restored after dialysis by infusion of salt-free albumin, and exogenous deoxycorticosterone and antidiuretic hormone were given. 2. Clearance studies in the period (3 h) after dialysis revealed no difference in the glomerular filtration rate or in the filtered sodium load between experimental and control rats but urinary sodium concentrations and absolute and fractional sodium excretion were significantly higher in the chloride-depleted group. 3. There was also a significant kaliuresis, increased urinary flow rate and diminished free water reabsorption. Urinary bicarbonate excretion increased to a variable degree but the major rise in anion excretion was ‘unmeasured’ (Na+ + K+ — [Cl− +HCO3− +PO43-]). 4. It is postulated that chloride depletion imposes limitations on sodium reabsorption in the ascending limb of the loop of Henle.

scholarly journals Erythrocyte membrane plaques from rats with magnesium deficiency

Blood ◽  
1977 ◽  
Vol 49 (4) ◽  
pp. 657-664 ◽  
Author(s):  
RJ Elin ◽  
HK Tan
Keyword(s):  
Erythrocyte Membrane ◽  
Plasma Membranes ◽  
Magnesium Deficiency ◽  
Freeze Fracture ◽  
Deficient Diet ◽  
White Rats ◽  
Dietary Magnesium ◽  
Freeze Fracture Electron Microscopy ◽  
And Control ◽  
Fracture Electron

Abstract This study investigated the anemia of dietary magnesium deficiency in inbred Fisher white rats using freeze-fracture electron microscopy. The plasma membranes of erythrocytes from animals receiving two different magnesium-deficient and control diets were observed at weekly or biweekly intervals for 6 wk. The earliest changes were small plaques on the external surface (ES) and fracture face (PF) of erythrocyte plasma membranes, which occurred after 2 wk of either magnesium-deficient diet. These plaques persisted and increased in size with progressive magnesium deficiency. When fully developed, the plaques consisted of round or oval elevations approximately 30–50 nm in diameter outlined by a narrow raised border. The surface of the plaques was smooth and devoid of intramembranous particles. Incubation of erythrocytes from magnesium-deficient rats in a physiologic solution containing 2 meq/liter magnesium for 1 hr at 37degrees C did not alter the appearance of the plaques. Erythrocytes from control rats, obtained during the same time periods, showed no plaques. Thus, a deficiency of magnesium in rats altered erythrocyte membrane structure.

Changes in the alkaline phosphatase (EC 3.1.3.1) and inorganic pyrophosphatase (EC 3.6.1.1) activities of rat tissues during magnesium deficiency. The importance of controlling feeding pattern

1976 ◽  
Vol 36 (3) ◽  
pp. 487-495 ◽  
Author(s):  
B. W. Loveless ◽  
F. W. Heaton
Keyword(s):  
Alkaline Phosphatase ◽  
Magnesium Deficiency ◽  
Protein Molecule ◽  
Feeding Pattern ◽  
Inorganic Pyrophosphatase ◽  
Rat Tissues ◽  
Eating Pattern ◽  
Adequate Diet ◽  
Tissue Extracts ◽  
And Control

1. The adoption of a meal-eating pattern of feeding by rats altered the alkaline phosphatase (EC 3.1.3.1) activity in serum and liver. It was therefore necessary to regulate the feeding pattern of both magnesium-deficient rats and control animals receiving a Mg-adequate diet in order to study the effect of the deficiency.2. Mg deficiency decreased the activities of alkaline phosphatase and inorganic pyro-phosphatase (EC 3.6.1.1) in serum, kidney and tibia, but increased them in spleen.3. Addition of a standard concentration of exogenous Mg to tissue extracts usually increased the activity of corresponding enzymes from Mg-deficient and control rats by the same proportion, indicating that the main effect of the deficiency was on the amount of enzyme present rather than on the efficiency of its operation.4. Certain quantitative differences in the response to exogenous Mg and the activity ratio, alkaline phosphatase: inorganic pyrophosphatase were found between tissues from Mg-deficient and control rats. The significance of these are discussed in relation to the association of the two enzymic activities with the same protein molecule, and the possible occurrence of isoenzymes.

Drug and Hormone Effects on Vitamin D Metabolism

Vitamin D ◽  
2018 ◽  
pp. 331-374
Author(s):  
Gregory R. Emkey ◽  
Sol Epstein
Keyword(s):  
Vitamin D ◽  
Vitamin D Metabolism ◽  
Hormone Effects

Electrolyte composition changes of chronically K-depleted rats after K loading

1987 ◽  
Vol 63 (2) ◽  
pp. 765-769 ◽  
Author(s):  
M. Sadre ◽  
H. P. Sheng ◽  
M. Fiorotto ◽  
B. L. Nichols
Keyword(s):  
Water Retention ◽  
Male Rats ◽  
Whole Body ◽  
Control Group ◽  
Elevated Plasma ◽  
Deficient Diet ◽  
Dose Control ◽  
And Control ◽  
Composition Changes ◽  
K Depletion

The responses of whole body, skeletal muscle, and plasma to oral K loading were studied in K-depleted male rats. Potassium depletion was induced by feeding the rats a K-deficient diet for 4 wk and injecting deoxycorticosterone acetate during the first week. After 4 wk, the rats were growth retarded and hypokalemic (1.9 mmol/l plasma) and had low whole-body and muscle K content, 188 +/- 27 and 276 +/- 19 mmol/kg fat-free dried tissue (FFDT), respectively, compared with 296 +/- 10 and 454 +/- 13 mmol/kg FFDT for the control group. Sodium and water retention also occurred in the K-deficient group. After K depletion, the rats were divided into four groups and received either 0, 1, 2, or 3 intragastric doses of 10 mmol KCl/kg at 8-h intervals. The rats were killed 8 h after the last dose. Control rats were treated similarly. K-depleted and control rats responded differently to K loading. In the normal rats, plasma K remained at 5.0 +/- 0.5 mmol/l, muscle K increased to 502 +/- 24 mmol/kg, and muscle K/N ratio increased from 3.0 to 3.4 mmol/g. In the K-depleted rats, plasma K increased to 7.2 +/- 0.7 mmol/l, muscle K increased to 453 +/- 50 mmol/kg, and muscle K/N ratio increased from 1.8 to 3.1 mmol/g. These data indicate that the capacity of the muscles to accumulate K was impaired after severe K depletion and caused elevated plasma K levels when repletion was complete.

Renal excretion of allantoin in rats: a micropuncture and clearance study

1977 ◽  
Vol 233 (5) ◽  
pp. F373-F381 ◽  
Author(s):  
J. P. Briggs ◽  
M. F. Levitt ◽  
R. G. Abramson
Keyword(s):  
Uric Acid ◽  
Renal Excretion ◽  
Rat Kidney ◽  
Chromatographic Technique ◽  
Experimental Conditions ◽  
Clearance Studies ◽  
Fluid Collections ◽  
And Control ◽  
Clearance Study ◽  
Column Chromatographic

Free-flow micropuncture and clearance studies were performed to evaluate the transport of allantoin inthe rat kidney. Inn all studies [2-14C]uric acid and [methoxy-3H]inulin were administered. With a two-step column chromatographic technique, radiolabeled uric acid and allantoin were separated in plasma, urine, and tubular fluid, and the [2-14C]allantoin concentration was determined. Tubular fluid collections were obtained under hydropenic and control coneated animals in the control and volume-expanded states. Clearance data were obtained in oxonic acid-treated animals under the same experimental conditions. These studies indicate that allantoin is not bound to plasma protein and is, therefore, freely filterable. Neither net reabsorption nor net secretion of allantoin was evident along the length of the nephron. The bubular handling of allantoin was demonstrated to be dissociated from that of uric acid in all experimental states. No significant intrarenal production of allantoin from uric acid was observed.

scholarly journals The effect of dietary zinc deficiency on pancreatic γ-glutamyl hydrolase (EC3.4.22.12) activity and on the absorption of pteroylpolyglutamate in rats

1989 ◽  
Vol 62 (1) ◽  
pp. 185-193 ◽  
Author(s):  
Mary C. Canton ◽  
B. M. Cotter ◽  
F. M. Cremin ◽  
P. A. Morrissey
Keyword(s):  
Zinc Deficiency ◽  
Pancreatic Enzyme ◽  
Hydrolase Activity ◽  
Zn Deficiency ◽  
Human Beings ◽  
Dietary Zinc ◽  
Deficient Diet ◽  
Adequate Diet ◽  
Plasma Folate ◽  
Male Wistar Rats

The effect of dietary zinc deficiency on γ-glutamyl hydrolase (EC3.4.22.12) activity and on pteroylpolyglutamate absorption was investigated in rats. Enzyme activity was determined in pancreas and gut lumen washings. Pteroylpolyglutamate absorption was studied by determining the rise in plasma folate levels following pteroylpolyglutamate ingestion. Two experiments were performed; in each purified diets were given to three groups of immature male Wistar rats for approximately 2 weeks. One group was given a Zn-deficient dietad lib.(ZD), the second was pair-fed daily with this group on a Zn-adequate diet (PF) and the third was given the Zn-adequate dietad lib.(AL). In Expt 1, significantly reduced pancreatic γ-glutamyl hydrolase activity was observed in ZD rats. In Expt 2, pteroylpolyglutamate was administered on day 14 and in the 3 h period following pteroylpolyglutamate ingestion, lumen γ-glutamyl hydrolase activity and plasma folate levels were significantly lower in ZD rats. Pancreas is reported as the source of lumen γ-glutamyl hydrolase in rats. The results presented indicate that the pancreatic enzyme is Zn-sensitive. It was concluded that, as a result, γ-glutamyl hydrolase activity was reduced in the lumen of ZD rats. Consequently the hydrolysis and subsequent absorption of pteroylpolyglutamate was impaired in ZD rats, as indicated by the smaller rise in plasma folate levels that occurred following pteroylpolyglutamate ingestion. Results of this study concur with previous observations in human beings and rats that Zn deficiency has an adverse effect on folate metabolism.

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