THE EFFECTS OF CALCITONIN AND PARATHORMONE ON PLASMA MAGNESIUM LEVELS BEFORE AND AFTER BIRTH IN THE RAT

1974 ◽  
Vol 61 (1) ◽  
pp. 1-13 ◽  
Author(s):  
J. M. GAREL ◽  
J. P. BARLET

SUMMARY Plasma magnesium levels measured in rats from 16·5 to 21·5 days of gestation and during the first week after birth proved to be invariably higher in the foetus than in the mother. The highest level observed was in the 16·5-day-old foetus. A small decrease occurred between 16·5 and 17·5 days of gestation; thereafter the plasma magnesium level did not change until 19·5 days and then decreased between 19·5 and 21·5 days. After birth an increase in plasma magnesium occurred with suckling but then remained constant during the first week of life. Parathyroid hormone (0·25 USP unit/g) injected into 21·5-day-old foetuses had no effect on plasma magnesium levels from 0·5 to 24 h after injection. This dose was found to be very potent in raising plasma calcium values 4 h after injection. In the 3-day-old newborn rat this dose was similarly ineffective. Removal of the foetal parathyroid glands by decapitation at 17·5 days of gestation was followed by a decrease in plasma magnesium at 21·5 days of gestation. Parathyroid hormone (0·25 USP unit/g) injected into decapitated foetuses did not change the level of magnesium in the plasma. Salmon calcitonin (S-CT) at two doses (0·4 and 4 ng/g) produced no effect on plasma magnesium concentrations in 3-day-old newborn rats 3 h after injection; whereas at both doses, marked diminutions in plasma calcium and phosphate concentrations were observed. After injection of 40 ng S-CT/g, plasma magnesium decreased in 3-day-old newborn rats 3 h after injection. This dose was found to decrease plasma magnesium in the 19·5-day-old foetus and in the 20·5-day-old foetus. Before 19·5 days of gestation no effect was observed.

1963 ◽  
Vol 61 (3) ◽  
pp. 411-415 ◽  
Author(s):  
N. S. Ritchie ◽  
R. G. Hemingway

1. Muriate of potash applied at rates of 0, 1 and 2 cwt./acre to herbage which had also received similar treatments in the previous year did not influence plasma magnesium or calcium values in lactating ewes.2. 24 Cheviot ewes had slightly lower plasma calcium and magnesium levels than 24 Half-bred ewes of the same age both before and after lambing.3. 6·6 g. of magnesium oxide given as a daily drench did not increase plasma magnesium values as measured by blood samples taken 24 hr. after drenching. Values were however increased by 0·5 mg. Mg/100 ml. four hours after drenching.4. No clinical cases of hypomagnesaemic tetany occurred, even although the mean plasma magnesium level of all the ewes in the experiment was only about 1·0 mg./lOO ml.5. Plasma magnesium values of ewes before lambing were significantly (P < 0·001) correlated with post-lambing levels. Values for the ewes during 1962 were equally significantly correlated with levels for the same sheep at comparable dates in 1961.


1997 ◽  
Vol 8 (4) ◽  
pp. 627-631
Author(s):  
K A Graham ◽  
N A Hoenich ◽  
M Tarbit ◽  
M K Ward ◽  
T H Goodship

Correction of acidosis in hemodialysis patients increases the sensitivity of the parathyroid glands to calcium. In this study, the parathyroid response to the correction of acidosis in eight hemodialysis patients was determined by performing dynamic assessment of parathyroid function before and after the correction of acidosis. The parathyroid response to intravenous calcitriol before and after the correction of acidosis was also assessed. After optimal correction of acidosis, there were no significant changes in blood pH, ionized calcium, phosphate, or alkaline phosphatase values, but the level of venous total CO2 increased significantly. Parathyroid hormone/ionized calcium curves were displaced downward after correction of acidosis, but not after the administration of intravenous calcitriol. The correction of metabolic acidosis in hemodialysis patients with secondary hyperparathyroidism can suppress parathyroid hormone secretion by increasing the sensitivity of the parathyroid glands to ionized calcium.


Plasma calcium is regulated with great precision: even large differences in diet change plasma calcium very little. McLean & Urist (1961) proposed that this constancy is achieved by appropriate alteration in the secretion rate of the parathyroid hormone. This hormone increases plasma calcium by increasing the rate of bone breakdown. Thus, a falling plasma calcium would stimulate the parathyroid glands to secrete more parathyroid hormone; a rising plasma calcium would produce inhibition of secretion. This hypothesis was first tested by Copp and colleagues in perfusion studies of the dog thyroid and parathyroid glands (Copp et al . 1962). Their results led them to postulate the existence of a new calcium-lowering hormone which they called calcitonin and which they thought came from the parathyroid glands. The existence of calcitonin was soon confirmed (Kumar, Foster & MacIntyre 1963). In experiments in the dog, the thyroid and parathyroid glands were perfused together in situ with blood of high and low calcium content. This was done without net addition or removal or calcium from the circulation (figures 20 and 21). There was a marked fall in systemic plasma calcium whenever the thyro-parathyroid glands were perfused with high-calcium blood (figure 22). This could have been due to inhibition of secretion of parathyroid hormone, but this explanation was excluded by control experiments. Complete removal of the thyroid and parathyroid glands produced little change in plasma calcium in the following two and a half hours (figure 23) in contrast to the marked hypocalcaemia accompanying thyro-parathyroid perfusion. Clearly a calcium-lowering substance was being liberated from the thyroid or parathyroid glands during high-calcium perfusion.


1972 ◽  
Vol 120 (559) ◽  
pp. 683-684 ◽  
Author(s):  
G. J. Naylor ◽  
Laura W. Fleming ◽  
W. K. Stewart ◽  
H. B. McNamee ◽  
D. Le Poidevin

There have been reports of the association of alterations in the divalent cation content of plasma with depressive illness. Coirault and colleagues (1959) found increased ionized calcium levels despite decreased total plasma calcium concentration in patients recovered from depression. More recently, Frizel and colleagues (1969) have reported normal plasma ionized and total calcium levels both before and after recovery from depression.


1969 ◽  
Vol 115 (529) ◽  
pp. 1375-1377 ◽  
Author(s):  
D. Frizel ◽  
Alec Coppen ◽  
V. Marks

Recent investigations suggest that there may be an abnormality of calcium and magnesium in depressive illness. Flach (1964) followed the urinary excretion of calcium in depressed patients maintained on a constant intake of calcium before and during recovery. Those patients that recovered showed a significant decrease in the excretion of calcium. Coiraultet al.(1959) reported an increase in ionized calcium and a decrease in total plasma calcium on recovery from depression. Cade (1964) reported considerably raised total plasma magnesium levels in depressed patients both before and after recovery. A connection between affective disorders and calcium metabolism is suggested by the common occurrence of such states in both hypo- and hypercalcaemia (Denco and Kaelbling, 1962; Rookus and Speelman, 1961). The present paper reports an investigation into total and ionized plasma calcium and magnesium in a group of depressed patients both before and after recovery. The effects of lithium carbonate, a compound used in the treatment and prophylaxis of affective disorders (Baastrup and Schou, 1967; Schou, 1963) on plasma concentrations of magnesium and calcium was also investigated.


1988 ◽  
Vol 117 (2) ◽  
pp. 261-271 ◽  
Author(s):  
C. P. Rodda ◽  
M. Kubota ◽  
J. A. Heath ◽  
P. R. Ebeling ◽  
J. M. Moseley ◽  
...  

ABSTRACT Parathyroid hormone (PTH)-like bioactivity, assayed as adenylate cyclase response in UMR 106-01 osteogenic sarcoma cells, was present in extracts of sheep fetal and maternal parathyroid glands and placenta. Preincubation of extracts with PTH(1–34) antiserum inhibited approximately 40% of the bioactivity in fetal parathyroid extracts, 50% in maternal parathyroid extracts, but only 10% of the bioactivity in the placental extract. Partial purification of placental extracts by chromatography yielded fractions containing PTH-like bioactivity which were similar in behaviour to that of PTH-related protein (PTHrP) from a human lung cancer cell line (BEN). An antiserum against synthetic PTHrP(1–16) partially inhibited the bioactivity of the placental extract and synthetic PTHrP(1–34), but had no effect on the bioactivity of bovine PTH(1–34) or bovine PTH(1– 84). The placental PTH-like bioactivity was higher in mid- than in late gestation. Fetal parathyroid glands contained the highest PTH-like bioactivity. Thyroparathyroidectomy of one fetal twin lamb in each of 16 ewes between 110 and 125 days of gestation resulted in decreases of the plasma calcium concentration and reversal of the placental calcium gradient that existed between the ewe and the intact fetus. Perfusion of the placenta of each twin in anaesthetized ewes was carried out sequentially with autologous fetal blood in the absence of the exsanguinated fetus. The plasma calcium concentration in the blood perfusing the placenta of each twin increased, but reached a plateau at a lower concentration in the perfusing blood of thyroparathyroidectomized fetuses than in that of the intact fetuses. Addition of extracts of fetal parathyroid glands or of partially purified PTHrP resulted in further increases in plasma calcium in the autologous blood perfusing the placentae of thyroparathyroidectomized fetuses, but addition of bovine PTH(1–84) or rat PTH(1–34) had no effect. The presence of this PTH-like protein in the fetal parathyroid gland and placenta may contribute to the relative hypercalcaemia of the fetal lamb. This protein, which is similar to PTHrP associated with humoral hypercalcaemia of malignancy, stimulates the placental calcium pump responsible for maintaining a relative fetal hypercalcaemia during gestation. J. Endocr. (1988) 117, 261–271


1965 ◽  
Vol 48 (1) ◽  
pp. 132-136 ◽  
Author(s):  
Heinrich G. Haas ◽  
Heinz Affolter ◽  
Ulrich C. Dubach

ABSTRACT In 1962 Copp et al. (1962) demonstrated a second, plasma calcium lowering factor from the parathyroid glands called calcitonin. These findings were subsequently confirmed by Kumar et al. (1963). Up to the present, however, calcitonin has not been demonstrated in man. In a patient with hypocalcaemic tetany the injection of a commercial parathyroid extract caused the same changes in plasma calcium as described by Copp et al. (1962) in dogs, i. e. an initial fall and a subsequent rise in the calcium level. In addition, changes in plasma magnesium paralleling those of calcium were also observed.


1978 ◽  
Vol 54 (4) ◽  
pp. 349-353 ◽  
Author(s):  
N. Nijs-De Wolf ◽  
N. De Nutte ◽  
H. Brauman ◽  
J. Corvilain

1. The parathyroid hormone-like biological activity of concentrated urine was measured by the increase of plasma calcium concentration after intravenous injection of the sample into chickens. 2. Urine was tested in hypoparathyroid patients, normal volunteer subjects, primary hyperparathyroid patients before and after surgery and patients with secondary hyperparathyroidism. 3. In primary and secondary hyperparathyroidism the biological activity was significantly higher than in urine from normal subjects, which was in turn significantly higher than the activity in the urine of hypoparathyroid patients. This bioactivity diminished after surgical removal of a hyperparathyroid adenoma. 4. Decreased activity after trypsinization indicated the peptidic nature of the hypercalcaemic substance.


1980 ◽  
Vol 239 (4) ◽  
pp. E255-E255

The effects of dopaminergic agonists on plasma levels of parathyroid hormone (PTH) have been studied in cattle. PTH increased within minutes in a dose-dependent manner during intravenous infusions of dopamine (DA) or epinine. Bromocriptine, in amounts that lowered plasma prolactin, inconsistently elevated PTH. Pimozide suppressed PTH responses to DA, whereas propranolol, phentolamine, phenylephrine, and atropine were ineffective. Plasma calcium and magnesium remained unaltered during DA and epinine infusions. Therefore DA appears to stimulate PTH secretion directly. After prolonged DA infusions, the secretion of PTH became resistant to both the administration of DA and isoproterenol, whereas the parathyroid glands remained responsive to a hypocalcemia. On the other hand, calcium suppressed PTH responses to DA. The results suggest that DA, beta-adrenergic agonists, and low calcium stimulate PTH secretion by separate but closely related mechanisms. Based on biochemical and histochemical observations on DA occurring in high amounts in bovine parathyroid glands, it is conceivable that this amine might stimulate PTH secretion at the level of the gland.


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.


Sign in / Sign up

Export Citation Format

Share Document