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ABSTRACT
In pregnant ewes bearing twin fetuses and fed an adequate Ca diet, the consequences of calcitonin (CT) deficiency (induced by thyroidectomy performed on day 30 of gestation, associated with daily thyroxine supplementation) differed according to the time of pregnancy. Such a deficiency had no significant effect either on fetal total body Ca content or on placental transfer of Ca in 77-day-old fetuses. On the contrary, CT deficiency for 110 days (on day 140 of pregnancy) was associated with an increased Ca concentration in fetal total body and increased placental transfer of Ca from the dam to its fetus, which did not occur in five thyroidectomized ewes supplemented with thyroxine and CT. This indicates that CT might protect the skeleton of the pregnant female against excessive demineralization by modulating placental transfer of Ca, when such a transfer becomes important, during periods of intense mineralization of the fetal skeleton.
J. Endocr. (1985) 104, 17–21
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ABSTRACT
The effect of ovine prolactin on intestinal Ca absorption and placental Ca transfer was studied in pregnant ewes. Six groups of five animals bearing a single fetus were used and injected s.c. daily between days 121 and 135. The first group was given 0·1 μg ovine prolactin/kg body wt per day, the second 0·1 μg ovine prolactin/kg body wt per day plus 0·1 μg 1α-hydroxycholecalciferol (1α-OH-D3)/kg body wt per day, the third 0 ·1 μg ovine prolactin/kg body wt per day plus 0·20 units calcitonin/kg body wt per day, the fourth 2 μg bromocriptine/kg body wt per day, the fifth 2 μg bromocriptine/kg body wt per day plus 0·1 μg ovine prolactin/kg body wt per day, and the sixth were controls injected with vehicle alone. The intestinal Ca absorption was measured on a duodenal loop tied off in vivo on day 136 and placental Ca transfer was evaluated between days 129 and 136. Ovine prolactin stimulated both intestinal Ca absorption and placental Ca transfer; these effects were further increased by 1α-OH-D3. Calcitonin had no effect on ovine prolactin-stimulated intestinal Ca absorption, but blunted the influence of ovine prolactin on Ca placental transfer. Bromocriptine decreased both intestinal Ca absorption and Ca placental transfer but these effects of bromocriptine were overcome by simultaneous injection of ovine prolactin.
J. Endocr. (1985) 107, 171–175
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SUMMARY
Purified porcine and salmon calcitonin and synthetic salmon and human calcitonin were infused at the rate of 20 MRC mu./kg/h over a 96 h period in intact male lambs. Every calcitonin preparation significantly increased the urinary excretion of inorganic phosphorus, sodium, potassium and calcium, while the urinary excretion of magnesium was always significantly inhibited. Similar significant effects were observed with purified porcine calcitonin in thyroparathyroidectomized lambs supplemented with thyroxine. Oxidation of calcitonin with performic acid completely abolished its effects on plasma calcium and on the kidney. It is concluded that, when used at physiological doses, in sheep calcitonin has an important effect on urinary excretion of inorganic phosphorus, sodium and magnesium.
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SUMMARY
The influence of injections of calcitonin on the hypercalcaemia and hyperphosphataemia induced by 1α-hydroxycholecalciferol (1α-OHD3) and 1,25-dihydroxycholecalciferol (1,25-(OH)2D3) was studied in growing lambs and lactating cows respectively.
In lambs, the hypercalcaemic and hyperphosphataemic effect of 0·1 μg 1α-OHD3/kg body weight (i.v.) was completely inhibited by 20 units calcitonin/kg body weight, injected subcutaneously in four equal doses at intervals of 12 h, the first injection of calcitonin occurring immediately after injection of 1α-OHD3. Moreover, the same dose of calcitonin partly inhibited the hypercalcaemia and hyperphosphataemia observed after injection of 0·25 μg 1α-OHD3/kg body weight.
In lactating cows, four injections of calcitonin (5 u./kg body weight each, at intervals of 12 h) prevented the rise of plasma calcium and phosphate levels occurring after injection of 1,25-(OH)2D3 (0·01 μg/kg body weight).
The results indicated that high plasma calcitonin levels can inhibit the hypercalcaemic and hyperphosphataemic effects of 1,25-(OH)2D3 in ruminants. Thus, hypocalcaemia might occur in parturient cows in spite of raised concentrations of 1,25-(OH)2D3 in plasma.
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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.
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ABSTRACT
The influence of 1,25-dihydroxycholecalciferol (1,25-(OH)2D3) on salivary inorganic phosphorus (Pi) concentration and secretion was studied in two groups of four heifers, the right parotid ducts of which were chronically fitted with a re-entrant cannula.
In four heifers i.v. Pi loading (5 mmol/min for 2 h) induced hyperphosphataemia associated with a decrease in plasma 1,25-(OH)2D concentration and an increase in salivary Pi concentration and secretion. In four other heifers, daily 1α-hydroxycholecalciferol injections (1 μg/kg body wt per day for 3 days) induced hyperphosphataemia associated with an increase in plasma 1,25-(OH)2D concentration and a decrease in salivary Pi concentration and secretion. These treatments had no significant effect on salivary calcium concentration and secretion.
Our results indicate that plasma 1,25-(OH)2D concentrations rather than phosphataemia regulate salivary Pi concentration and secretion in cattle.
J. Endocr. (1987) 112, 427–430
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ABSTRACT
Plasma concentrations of atrial natriuretic peptide (ANP), plasma renin activity (PRA), plasma concentrations of aldosterone, urine flow rate and sodium and potassium excretion were studied in two groups of four conscious 3-day-old male calves, infused with hypertonic saline or vehicle. Hypertonic saline infusion (20 mmol NaCl/kg body weight) was accompanied by a progressive rise in plasma concentrations of ANP (from 16·5 ± 0·2 pmol/l at time 0 to 29·3 ± 3·0 pmol/l at 30 min; P< 0·05) and by a gradual decrease in PRA (from 1·61±0·23 nmol angiotensin I/1 per h at time 0 to 0·54± 15 nmol angiotensin I/1 per h at 90 min; P<0·05); there was no change in the plasma concentration of aldosterone. Within the first 2 h of the 24-h urine collection period there was a marked rise in urine flow rate and sodium excretion in treated calves when compared with control animals (66·0 ± 8·3 vs 15·9±1·2 ml/kg body weight per 2 h (P<0·05) and 6·7±1·3 vs 0·4±0·02 mmol/kg body weight per 2 h (P<0·01) respectively). During the following 22 h, urinary water and sodium excretion remained at significantly high levels.
Thus, in the conscious newborn calf, changes in plasma ANP levels and urinary water and sodium excretion during hypertonic saline infusion are compatible with the hypothesis that endogenous ANP participates, at least in part, in the immediate diuretic and natriuretic renal response induced by the sodium overload.
J. Endocr. (1988) 119, 23–29
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ABSTRACT
Plasma concentrations of atrial natriuretic peptide (ANP) were studied in eight adult non-pregnant cows and in two groups of six chronically catheterized bovine fetuses and their mothers in the eighth month of pregnancy. The first group of fetuses was used for studying the effect of an acute i.v. sodium load (240 mmol NaCl/fetus) on fetal ANP; the second group acted as controls. The mean basal ANP levels in the third-trimester bovine fetus were three to four times higher than maternal values (39·5 ± 5·5 and 9·4 ± 0·6 pmol/l respectively; P<0·01). Basal maternal plasma ANP levels were twice as high in pregnant cows in the third trimester of pregnancy than in non-pregnant cows (9·4 ± 0·6 and 4·3 ± 0·7 pmol/l respectively; P<0·05).
In response to an i.v. hypertonic saline injection, fetal plasma ANP levels increased significantly (P<0·01) to a maximum of 86·7± 17·6 pmol/l 10 min after the injection, and returned to baseline within 60 min after the treatment; during the 20 min following the i.v. sodium load, fetal plasma ANP correlated significantly with fetal plasma sodium concentrations (r 0·96; n=12) and with fetal plasma osmolality (r =0·94; n=12). No significant changes in maternal ANP values were observed in the two groups of animals.
These results suggest that ANP secretion is stimulated during pregnancy in cows, and that, in the bovine fetus, a hypertonic sodium load appears to be a potent stimulus for ANP release.
Journal of Endocrinology (1989) 121, 5–9
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I.N.R.A. Theix, 63110 Beaumont, France, and *Department of Animal Physiology and Nutrition, The University of Leeds, Leeds, LS5 3HL, England
(Received 3 May 1974)
It has been demonstrated that histamine injections in guinea-pigs cause peptic ulceration and death from peritonitis secondary to perforation of the ulcer and that the thyroid gland of these animals contains a non-thyroxine factor which regulates gastric HCl secretion (Watman & Nasset, 1949, 1951) and which protects against gastric ulceration. Thus we have investigated the effect of porcine calcitonin (P-CT) given intragastrally on histamine-induced peptic ulcer and gastric HCl secretion in guinea-pigs.
In the first experiment 18 young black and white male (180–200 g) guinea-pigs were used. They were given food and water ad libitum throughout the experiment. Twelve of them were surgically thyroidectomized (TX) (with preservation of the parathyroid glands) 10 days before the beginning of the experiment. These animals were supplemented with thyroxine (T4)
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ABSTRACT
The influence of synthetic parathyroid hormone related peptide (PTHrp) fragments on placental transfer of Ca was studied in four groups of four single ovine fetuses fitted with catheters chronically implanted into their left jugular vein (for injections) and carotid artery (for blood sampling), and used between days 104 and 118 of gestation. The first group received PTHrp(1–34), the second PTHrp(107-138), the third bovine PTH(1–34), and the last (control) group was injected with solvent alone. Each peptide (6 nmol/fetus per day) was injected i.v. three times per day from day 105 until day 116 of gestation. Placental Ca transfer (mmol/24 h per kg fetal wt) from the dam to the fetus was not different in control fetuses 7·1±0·6) and those given PTHrp(107–138) (7·2±0·5), but it was significantly increased by bovine PTH(1–34) (8·6±0·4; P < 0·05) and by PTHrp(1–34) (10·1±0·3; P < 0·01). Both peptides also significantly increased plasma concentrations of 1,25 dihydroxy-vitamin D3 (1,25-(OH)2D). These results indicate that PTHrp(1–34) can stimulate placental Ca transfer by increasing 1,25-(OH)2D synthesis, but also possibly by acting directly upon the placenta.
Journal of Endocrinology (1990) 127, 33–37
