Nature of calcemic effect of 1,25-dihydroxyvitamin D3 in experimental hypoparathyroidism

1983 ◽  
Vol 244 (4) ◽  
pp. E313-E316
Author(s):  
E. Hefti ◽  
U. Trechsel ◽  
H. Fleisch ◽  
J. P. Bonjour

The influence of 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] treatment on the daily fluctuation of plasma calcium concentration ( [Ca]P1) in relation to the feeding-fasting alternation has been studied in vitamin D-replete sham-operated (sham) and thyroparathyroidectomized (TPTX) rats fed a normal Ca diet. 1,25(OH)2D3 was given (26 or 39 pmol/day) intraperitoneally either by single injection or constant infusion using osmotic minipumps. After 7 days of treatment [Ca]P1 was measured at 4-h intervals for 24 h. Pair-fed, sham and TPTX animals received the solvent vehicle intraperitoneally. The results show that in sham rats the very moderate daily fluctuation of [Ca]P1 was not accentuated by 1,25(OH)2D3. A marked fluctuation of [Ca]P1 in relation to the food intake was observed in untreated TPTX as compared with sham rats. In TPTX rats 1,25(OH)2D3 increased the fasting [Ca]P1. In contrast the rise in [Ca]P1 during feeding was not significantly accentuated by 1,25(OH)2D3. The daily fluctuation of [Ca]P1 was the same whether the dose of 1,25(OH)2D3 was given in one single injection or by constant infusion, suggesting that this hormone is not involved in the hour-to-hour regulation of [Ca]P1. In conclusion, in the absence of parathyroid glands, 1,25(OH)2D3 given in doses that stimulate intestinal calcium absorption has a much more pronounced effect on the fasting calcemia than on the rise in calcemia observed during the feeding period. These results suggest that the mobilization of calcium from bone could play an important role in the calcemic effect of 1,25(OH)2D3 when given in the hypoparathyroid state.

1985 ◽  
Vol 107 (3) ◽  
pp. 389-395 ◽  
Author(s):  
S. Lausson ◽  
J. F. Staub ◽  
G. Milhaud ◽  
A. M. Perault-Staub

ABSTRACT Circadian fluctuations of plasma calcium and immunoassayable calcitonin levels were studied in normal and calcium-deficient 2-month-old rats. The relationship between these parameters was also studied in animals which had been fasted for short periods. The plasma calcium rhythm persisted and was even amplified in rats placed on a 4-week calcium-deficient diet. In these rats, as in normal rats, the plasma calcium concentration diminished during the dark period. Calcitonin levels increased at the onset of the feeding period in normal rats but, in calcium-deficient rats, the pattern changed completely, with a major peak at the end of the light period and remaining at a low level during the dark feeding period. This modification of calcitonin rhythmicity appeared to be dependent on the degree of calcium deficiency. Fasting had little effect on calcitonin rhythms in either normal or calcium-deficient rats. It is concluded that the calcitonin rhythm is relatively independent of feeding per se and that there appears to be no simple relationship between plasma calcium and calcitonin concentrations. It is suggested that the results may best be interpreted as reflecting the presence of rhythmic endogenous phenomena which are intrinsic to calcium metabolism and its regulation in the rat. J. Endocr. (1985) 107, 389–395


1981 ◽  
Vol 60 (1) ◽  
pp. 101-107 ◽  
Author(s):  
R. Rizzoli ◽  
K. Hugi ◽  
H. Fleisch ◽  
J.-P. Bonjour

1. Chronic administration of 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] can normalize plasma calcium in human hypoparathyroidism and in thyroparathyroidectomized animals. The effect of 1,25(OH)2D3 on plasma calcium is associated with an increase in urinary calcium excretion. In an attempt to prevent this increase, thyroparathyroidectomized rats receiving 1,25(OH)2D3 were also treated with hydrochlorothiazide for 9–11 days. 2. Calcium clearance studies show that hydrochlorothiazide stimulated the tubular reabsorption of calcium in thyroparathyroidectomized rats treated with 1,25(OH)2D3. 3. Calcium balance and kinetic studies indicated that hydrochlorothiazide decreased 1,25(OH)2D3-induced hypercalciuria in thyroparathyroidectomized rats. Hydrochlorothiazide did not affect the 1,25(OH)2D3-induced increase in plasma calcium. The hypocalciuric effect of hydrochlorothiazide was not associated with significant changes in calcium deposition into or release from bone. 4. In thyroparathyroidectomized rats treated with 1,25(OH)2D3 the hypocalciuric effect of hydrochlorothiazide was associated with a fall in intestinal calcium absorption. Overall, the calcium balance was unaffected. 5. Thus it appears that hydrochlorothiazide reduces the 1,25(OH)2D3-induced hypercalciuria in parathyroid hormone-deficient animals by decreasing intestinal calcium absorption. Despite the decreased absorption, hydrochlorothiazide does not reduce the 1,25(OH)2D3-induced increase in plasma calcium.


1977 ◽  
Vol 233 (3) ◽  
pp. E160 ◽  
Author(s):  
R Rizzoli ◽  
H Fleisch ◽  
J P Bonjour

Thyroparathyroidectomy (TPTX) decreases plasma calcium, bone formation and resorption, and tubular reabsorption of calcium. It also reduces the production of 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3] which very likely results in the decrease in the intestinal calcium absorption (Vna) observed after TPTX. We have examined whether the influence of TPTX on plasma calcium and bone calcium fluxes could be corrected by doses of 1,25-(OH)2D3 (2 X 13 pmol/day ip), which just normalize Vna. The study was made by calcium balance and 45Ca kinetics in rats receiving a normal supply of vitamin D3. The results show that in TPTX rats physiological doses of 1,25-(OH)2D3 increased plasma calcium and decreased plasma phosphate. Calcium retention was not fully corrected because 1,25-(OH)2D3 increased urinary calcium excretion. The deposition into and the release of calcium from bone were enhanced by 1,25-(OH)2D3 but remained lower than in pair-fed sham-operated animals. Thus, in as much as the diminished renal production of 1,25-(OH)2D3 in TPTX is entirely responsible for the reduced Vna, the decrease in 1,25-(OH)2D3 could only partly explain the effect of thyroparathyroidectomy on bone calcium fluxes.


1970 ◽  
Vol 64 (1) ◽  
pp. 150-158 ◽  
Author(s):  
S. Pors Nielsen

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.


1984 ◽  
Vol 67 (6) ◽  
pp. 613-618 ◽  
Author(s):  
B. F. Robinson ◽  
R. J. W. Phillips

1. The effect of a small increase in local plasma calcium concentration on the responsiveness of the forearm resistance vessels to verapamil has been examined in normal subjects, by using a plethysmographic method with infusion of calcium and other agents into the brachial artery. 2. Infusion of calcium at a rate which increased the concentration in forearm venous blood by about 0.5 mmol/l caused basal blood flow to fall by 19% and the dilator response to verapamil to fall by 35% (n = 8; P<0.02). 3. When, after 46 min, the infusion of calcium was discontinued, the dilator response to verapamil increased to reach a level 53% higher than the initial control (n = 8; P<0.02). 4. Infusion of calcium had no effect on the dilator response to sodium nitroprusside. 5. Infusion of noradrenaline at a rate which caused a greater reduction in basal flow than that induced by calcium had no effect on the response to verapamil. 6. It is concluded that the dilator response to verapamil, which is thought to reflect activity of the potential operated system for calcium entry, is selectively depressed by a small elevation of plasma calcium concentration, but subsequently becomes elevated. These findings point to an important role for calcium in the regulation of membrane function in the resistance vessels and support the view that altered calcium handling may contribute to the development of primary hypertension.


1994 ◽  
Vol 72 (7) ◽  
pp. 764-770 ◽  
Author(s):  
N. Krishnamra ◽  
K. Angkanaporn ◽  
T. Deenoi

Absorptive and secretory capacities of six in situ intestinal loops of equal length were compared under the same calcium load and calcemic condition. The highest rate of calcium absorption was found in duodenum, colon, and proximal jejunum when loops were filled with 0.3 mM calcium, and in duodenum and proximal jejunum when filled with 10 mM luminal calcium. Secretory rates were in the following order: duodenum, jejunum, proximal jejunum, cecum, ileum, and proximal colon. Absorption of 0.3 mM calcium was decreased in all but the cecum and colon during hypercalcemia, and in duodenum, proximal jejunum, and colon during thyroparathyroidectomy-induced hypocalcemia. In contrast, calcium secretion was directly related to plasma calcium concentration and the length of the intestine. Functional resection of any part met with a compensatory increase in calcium absorption by the remaining segments, with the exception of the resection of the distal ileum with the large bowel. In conclusion, proximal small intestine exhibited the highest rate of absorption and secretion, but functional resection of this or any part did not affect the overall calcium absorption if luminal calcium was 10 mM. Moreover, enhanced secretion and reduced absorption during hypercalcemia were beneficial with respect to plasma calcium regulation.Key words: calcium, hypercalcemia, hypocalcemia, intestinal absorption, intestinal secretion.


1999 ◽  
Vol 14 (1) ◽  
pp. 57-64 ◽  
Author(s):  
E. M. Colin ◽  
G. J. C. M. Van Den Bemd ◽  
M. Van Aken ◽  
S. Christakos ◽  
H. R. De Jonge ◽  
...  

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