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PubMed1982

Involvement of calcium in calcitonin induced stimulation of glycolysis in rat kidney in situ.

The effects of intravenous salmon calcitonin on tissue carbohydrate and redox metabolism were studied in rat kidney in situ and were compared to the effects of EGTA infusion. Calcitonin (0.8 MRC U, in bous) caused, after 10-20 min, a reductive shift of the cytosolic NAD redox pair, and an oxidative shift of the mitochondrial NAD redox pair. It also caused a stimulation of glycolysis with the cross-over between phosphoenolpyruvate and pyruvate. These results were reproduced by treatments of hypocalcemia with EGTA or with thyroparathyroidectomy. Most of the effects were opposite in direction to the reported effects of CaCl2 and parathyroid hormone. The above results suggest that in kidney calcitonin causes a stimulation of pyruvate kinase, and/or inhibition of phosphoenolpyruvate carboxykinase, and that the effects are related to changes in the intracellular calcium.

Animals↗
PubMed1985

Insulin modulates the stimulation of renal 1,25-dihydroxyvitamin D3 production by parathyroid hormone.

Previous studies have shown that there is an impairment in renal production of 1,25-dihydroxyvitamin D3 (1,25(OH)2D3), the major biologically active metabolite of vitamin D3, in diabetes. This impairment is not due to a deficiency in the parathyroid hormone (PTH), a major stimulator of renal 1,25(OH)2D3 production. Therefore, we have investigated the capacity of PTH to stimulate 1,25(OH)2D3 production in insulin deficiency and with insulin replacement. Experiments were performed in rats fed a 0.6% calcium, vitamin D sufficient diet for 2 weeks. Thyroparathyroidectomy was performed on all rats. Rats to be rendered diabetic were injected with streptozotocin immediately after surgery. In non-diabetic rats, PTH administration significantly increased renal 1,25(OH)2D3 production (11 +/- 2 vs 46 +/- 5 pg/min/g; P less than 0.05). In diabetic rats, however, PTH caused only a modest increase in 1,25(OH)2D3 production (11 +/- 1 vs 19 +/- 4 pg/min/g; P less than 0.05). With insulin replacement, PTH stimulation of 1,25(OH)2D3 production was markedly increased over that seen in diabetic rats (48 +/- 12 vs 19 +/- 4 pg/min/g; P less than 0.05). PTH was equally effective in raising serum calcium, depressing serum phosphorus and tubular reabsorption of phosphate in non-diabetic as well as in diabetic rats. These results demonstrate that insulin is necessary for the maximal stimulation of renal 1,25(OH)2D3 production by PTH. However, insulin is not necessary for PTH action in terms of renal handling of phosphate and inducing hypercalcaemia. These results suggest multiple pathways for the action of PTH, only some of which are insulin requiring.

Animals↗
PubMed1997

Starvation-induced increase in the parathyroid hormone/PTH-related protein receptor mRNA of bone and kidney in sham-operated and thyroparathyroidectomized rats.

Parathyroid hormone (PTH) acts on bone and kidneys by binding to PTH/PTH-related protein (PTHrP) receptors and regulating calcium (Ca) and phosphorus (P) homeostasis. PTH/PTHrP receptor mRNA was expressed at high levels in PTH target tissues such as the kidneys and bone including the calvaria, femur, and tibia. Because short-term starvation influences Ca and P ion homeostasis, we measured changes in PTH/PTHrP receptor mRNA expression in the bone and kidneys. Food deprivation for 3 days decreased the serum Ca and P concentrations, and reinstitution of feeding for 2 days normalized the serum Ca level and significantly increased the serum P level. Concomitantly, rat immunoreactive PTH (riPTH) was increased during starvation and returned to the control level after 2 days of subsequent feeding. Serum 1 alpha, 25-dihydroxyvitamin D3 (1,25(OH)2D3) concentrations did not significantly change during starvation and subsequent feeding. Starvation up-regulated PTH/PTHrP receptor mRNA expression in both bone and kidney. The effects of food deprivation on the receptor transcript abundance were greater in bone (threefold increase compared with control) than in the kidney (1.8-fold increase), whereas the mRNA level increase by food deprivation was more rapid in the kidneys than in bone. The PTH-induced adenylyl cyclase activity of renal membranes increased in starvation. Feeding after starvation normalized the mRNA levels in both tissues. Serum PTH depression, initiated by thyroparathyroidectomy, did not affect PTH/PTHrP receptor mRNA levels in bone and kidney in rats that were fed or starved for 3 days. The abundance of receptor mRNA in bone and kidney was significantly lower in fed rats given either corticosterone or vehicle than in starved rats. These data indicate that starvation induces PTH/PTHrP receptor mRNA expression in bone and kidney, independently of serum PTH and corticosterone concentrations. The factors leading to up-regulated receptor mRNA induced by starvation remain unknown.

Adenylyl Cyclases↗
PubMed1975

Effect of calcium deprivation on parathyroid hormone-mediated bone and kidney contributions to the maintenance of plasma calcium in rats.

This study was designed to investigate the roles of bone and kidney in the acute regulation of plasma calcium by parathyroid hormone (PTH) during prolonged calcium deprivation. The effect of PTH was assessed by gland ablation. Animals were thyroparathyroidectomized or sham-operated and their urine was collected for 3 h. Subsequently they were anaesthetized and bled from the abdominal aorta. In rats fed on a low calcium diet, urinary hydroxyproline excretion was enhanced and, unlike animals fed on a normal diet, decreased 3 h after thyroparathyroidectomy (TPTX). In addition TPTX decreased plasma calcium by 0-45 mg/100 ml in normal rats compared with 1-94 mg/100 ml in animals fed on a calcium-deficient diet. Urinary calcium increased by 161 and 12 mug and accounted for 82 and 1-4 % of the fall in plasma calcium in normal and calcium-deprived animals respectively. The corresponding contributions of bone were 18 and 98-6%. These findings support the view that with prolonged calcium deprivation in adult rats, the relative contributions of bone and kidney to the acute regulation of the plasma calcium level by PTH are reversed. As a result, bone rather than kidney becomes the more important organ. At the same time non-PTH-mediated kidney reabsorption of calcium is increased.

Animals↗
PubMed1976

Pituitary-adrenal function in thyroparathyroidectomized male and female rats.

The influence of thyroid hormones on pituitary-adrenal function was assessed by studying several aspects of adrenocortical function approximately 30 days after thyroparathyroidectomy (TPTx). Both male and female rats showed evidence of rhythmic adrenocortical activity; peak plasma corticosterone levels occurred just before the dark phase of the lighting schedule. Only the amplitude of the rhythm appeared altered by TPTx. Peak plasma corticosterone levels in TPTx male and female animals were less (P less than 0.05) than corresponding levels in intact control rats. Both sexes showed significant responses to stress, but the morning stress response in TPTx females was less (P less than 0.01) than the stress response in intact controls. Concomitant with the reduced stress response, the adrenocortical response to exogenous ACTH was reduced in TPTx female rats.

Adrenal Glands↗
PubMed1988

Thyroid and parathyroid-independent increase in plasma 1,25-dihydroxyvitamin D during late pregnancy in the rat.

The effect of thyroparathyroidectomy (TPTX) on the plasma concentrations of the vitamin D metabolites (25-(OH)D, 24,25-(OH)2D and 1,25-(OH)2D) has been studied in pregnant rats and their fetuses during the last quarter of gestation. Maternal and fetal vitamin D metabolites were not significantly affected by TPTX. A significant increase in plasma 1,25-(OH)2D concentrations was observed in both TPTX and control mothers and fetuses from days 19 to 21. Fetal and maternal plasma 25-(OH)D were positively correlated in both control and TPTX groups. Such a correlation was also found for 24,25-(OH)2D in the two groups. In contrast, a positive correlation between maternal and fetal plasma concentrations of 1,25-(OH)2D was found in TPTX but not in control rats. These data suggest that major alterations in calcium metabolism, such as that produced by maternal TPTX, are insufficient to affect the changes in maternal and fetal plasma 1,25-(OH)2D during late pregnancy significantly. They also suggest that parathyroid hormone, thyroxine, and/or calcitonin may control a possible placental transfer of 1,25-(OH)2D in the rat.

24,25-Dihydroxyvitamin D 3↗
PubMed1988

Evidence for a novel parathyroid hormone-related protein in fetal lamb parathyroid glands and sheep placenta: comparisons with a similar protein implicated in humoral hypercalcaemia of malignancy.

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.

Animals↗
PubMed2006

Hypertensive effect of calcilytic NPS 2143 administration in rats.

Secretion of parathormone (PTH), the main parathyroid hormone, which is under the control of the calcium sensing receptor, might be inhibited by calcimimetics and stimulated by calcilytics. Parathyroid glands also secrete parathyroid hypertensive factor. Recently, it was shown that calcimimetic NPS R-568 induced decreased blood pressure in spontaneously hypertensive rats (SHR) in the presence of parathyroid glands. Therefore, the aim of this study was to determine whether administration of the calcilytic NPS 2143 provoked an increase of mean arterial blood pressure (MAP) in normotensive rats. We used male Wistar rats anaesthetized with thiopental. Clearance experiments were performed and the effect of bolus, 1 mg/kg body weight i.v. of NPS 2143 on MAP in the presence and absence of thyroparathyroidectomy (TPTX) was monitored continuously. Calcilytic properties of NPS 2143 were confirmed directly by a significant (P < 0.05) increase of plasma PTH concentration, and indirectly by a rise of plasma Ca(2+) concentration and urinary fractional phosphate excretion (FE Pi). NPS 2143 administration markedly (P < 0.05) increased MAP, calculated as the difference ( Delta ) in MAP between sequential measurements and the time of bolus injection of calcilytic. The observed increase of blood pressure in the NPS 2143 group was also significant (P < 0.05) compared with the control group. Performance of TPTX prevented the hypertensive effect of NPS 2143. We conclude that NPS 2143 is responsible for increased blood pressure in rats in the presence of parathyroid glands.

Animals↗
PubMed1992

Dopamine enhances the phosphaturic response to parathyroid hormone in phosphate-deprived rats.

Phosphate deprivation results in a resistance to the phosphaturic effect of parathyroid hormone. Dopamine is phosphaturic and is synthesized by kidney proximal tubule, the nephron subsegment where parathyroid hormone inhibits phosphate transport. Thus, to test the hypothesis that phosphate deprivation is associated with low intrarenal dopamine synthesis and that dopamine infusion will overcome the resistance to the phosphaturic response to parathyroid hormone, the following study was performed. The effect of dietary phosphate intake on intrarenal dopamine synthesis, as reflected by urinary dopamine excretion, was determined. Rats were placed in metabolic cages (N = 5) and were fed a low-phosphate diet (0.07% Pi) for 4 days and then a high-phosphate diet (1.8% Pi) for 4 days. Twenty-four-hour urinary dopamine excretion was significantly lower in rats fed a low-phosphate diet (2.53 +/- 0.06 versus 4.10 +/- 0.30 micrograms/day). Further, the effect of dopamine infusion on the blunted phosphaturic response to parathyroid hormone was studied in rats fed a low-phosphate diet for 1, 2, and 3 days. Control clearances were taken 2 h after thyroparathyroidectomy; then, parathyroid hormone (33 U/kg plus 1 U/kg/min), dopamine (25 micrograms/kg/min), or parathyroid hormone plus dopamine were infused for 60 min. Changes in the fractional excretion of phosphate were significantly greater in rats fed a low-phosphate diet infused with parathyroid hormone plus dopamine than in rats fed a low-phosphate diet infused with parathyroid hormone alone (delta 27.9 +/- 5.8 versus 11.2 +/- 2.6% for day 1; 28.4 +/- 1.4 versus 7.1 +/- 3.6% for day 2; and 10.7 +/- 2.8 versus -0.2 +/- 0.2% for day 3; N = 5 for all groups).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Renal and intestinal Pi transport adaptation to low phosphorus diet in uremic rats.

The normal response of the kidney and intestine to a low-phosphorus diet (LPD) is an increased rate of Na(+)-dependent Pi transport by their brush border membranes (BBM). Dietary phosphorus restriction is used to reduce Pi accumulation in chronic renal failure. It is not known, however, if the uremic state alters the adaptive responses to an LPD. The adaptive response of the renal and intestinal BBM vesicles (BBMV) to LPD in acutely uremic (NX) and sham-operated (SH) control rats placed on a normal diet or an LPD was studied. In renal BBMV, the initial Na+ gradient-dependent Pi transport was lower in NX than in SH rats. Na(+)-independent uptake was unchanged. Thyroparathyroidectomy did not reverse the reduced Pi transport in NX rats. Kinetic studies showed a reduction of the apparent Vmax for Pi in BBMV from NX compared with SH rats (738 +/- 69 and 1,078 +/- 90 pmol/5 s.mg for NX and SH rats, respectively; P < 0.05; N = 5) with no change in the apparent Km. In intestinal BBMV, the initial Na+ gradient-dependent Pi transport was not different between SH and NX rats. There was also no difference in Pi transport kinetics between SH and NX rats. The adaptive response to an LPD persisted in renal and intestinal BBMV from NX rats and was comparable to that observed in SH rats: +54% for SH versus +48% for NX rats in kidney BBMV and +70.2% for SH versus +71.8% for NX rats in intestinal BBMV.(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptation, Physiological↗
PubMed1998

SEM study of the development of rat incisor enamel hypoplasia under hypocalcemia induced by thyro-parathyroidectomy.

Several clinical studies have reported the presence of enamel hypoplasia in congenital hypoparathyroidism or hypocalcemia. In previous studies we showed that thyroparathyroidectomy (TPTX) induced perturbations of the ameloblast morphology and secretion, of the rod pattern and of the enamel surface at late secretory stage and beginning of maturation, and limited hypoplasia in the erupted enamel of rat incisor. The aim of the present study was to evaluate by SEM, the extent and evolution of the enamel alterations of thyro-parathyroidectomized rats during the maturation stage. Wistar rats were thyro-parathyroidectomized and sacrificed 57 days later. The incisors were dissected out and processed for SEM. The surface of the incisor was observed from the end of secretion/beginning of maturation to its incisal erupted end. Transverse sections were prepared to study the structural defects and the prism pattern at different stages. The results showed that the surface of the TPTX incisors presented large hypoplastic defects at the end of secretion/beginning of maturation and only small defects in the erupted part. Transverse sections showed that, at the transition from secretion to maturation, the enamel defects extended to the mid-thickness of the tissue. At the incisal end the defects were limited to the outer enamel. As it is difficult to understand how the large apical defects could recover to appear as small hypoplasia at the incisal end, these results raise new questions concerning: (1) the effect of a long term calcium deficiency upon the cellular activity of the ameloblasts, and (2) the capacity of the enamel organ to compensate structural abnormalities.

Animals↗
PubMed1988

Leucine catabolism and incorporation into tissue proteins in thyroparathyroidectomized rats.

We investigated parameters of leucine metabolism in thyroparathyroidectomized (TPX) and pair-fed control rats using a technique of continuous infusion of [l-14C]leucine. The rate of leucine turnover was significantly smaller in TPX than in control rats (42.5 +/- 2.6 vs 35.1 +/- 1.9 mumole/hr/100 g, mean +/- SEM, six rats). There was no significant difference between rates of alpha-decarboxylation of leucine by the two groups of rats. The protein incorporation of leucine was significantly smaller in the muscle of TPX than control rats (39 +/- 5 vs 24 +/- 4 pmole/mg protein, mean +/- SEM, six rats) but in liver it was not significantly different. Thyroparathyroidectomy also had no significant effect on concentration of either leucine or its ketoacid (alpha-ketoisocaproate) in plasma, liver, and muscle. We conclude that hypothyroidism does not alter catabolism of leucine but reduces its incorporation into muscle protein.

Animals↗
PubMed1976

Tubular adaptation of inorganic phosphate (Pi) transport in response to variations in dietary Pi in rats.

The renal response to variations in the dietary intake of inorganic phosphate (Pi) has been studied in intact and thyroparathyroidectomized (TPTX) rats. The results show that the renal tubule can markedly vary its capacity to transport Pi according to homeostatic requirements: the lower the prior dietary intake, the higher the capacity of the tubule to reabsorb Pi. This adaptive response also occurs in TPTX rats. It is observed as early as three days after varying the dietary intake of Pi. This diet-induced difference in the tubular transport capacity for Pi can be seen in the presence of identical plasma Ca and urinary pH and also during marked expansion of extracellular volume. Comparison between Pi intake and thyroparathyroidectomy indicates that the fractional excretion of Pi measured at similar [Pi] Pl. can vary more than 100 times according to the prior dietary intake, whereas the removal of the thyroparathyroid glands brings about only a change of 2-4 times in this parameter. Free-flow micropunctures done in sham-operated rats pair-fed diets containing either 0.2 or 1.8 g/100 g P show a difference in Pi handling along the early proximal and distal tubule. However the most striking alteration seems to take place along the terminal nephron where an apparent net secretion of Pi would occur in the rats fed the high Pi diet. In conclusion the renal tubule adapts its transport capacity for Pi according to the supply of Pi in the diet. This involves a PTH-independent mechanism of great adaptive capability.

Administration, Oral↗
PubMed1976

Urinary phosphate excretion after total thyro-parathyroidectomy in thyroid carcinoma.

It is well established that deficiency of parathyroid hormone causes an increase of the tubular reabsorption of inorganic phosphate. Earlier evaluations, however, are based on animal experiments or in clinical studies where the degree of a postoperative hypoparathyroidism is not clearly defined. Eight patients with thyroid cancer have been operated on with a total thyroparathyroidectomy, biopsy of all identified parathyroids and autotransplantation of these glands. During a postoperative period of 3-5 days there is an arrest of the paraghyroid function before the glands have a new vascular supply. The levels in the serum and urine of calcium, phosphate, sodium, potassium, magnesium, chloride and creatinine were recorded. The excretion of phosphate diminished to unmeasurable values, indicating a complete tubular reabsorption of phosphate. After 5-6 days, when the autografted parathyroids began to function, phosphate reappeared in the urine together with a slow increase in S-Ca. No substitution with calcium or vitamin D was given in the postoperative period.

Adult↗
PubMed1975

[The morphology and function of rat C-cells. 4. Determination of calcium, inorganic phosphorus and total nitrogen in the femora of untreated parathyroidectomized or thyreoparathyroidectomized and hormonally substituted female rats].

Female Wistar rats of a live weight of about 160 g and fed with a standard laboratory diet, were parathyroidectomized, or thyroparathyroidectomized and treated with thyroxine, parathyroid hormone, calcitonin. thyroxine and parathyroid hormone, or thyroxine and calcitonin. On the 15th day post operationem, and after twelve days of hormone treatment, the concentrations of calcium, inorganic phosphorus and total nitrogen were determined in the femur bone. Parathyroidectomy resulted in a decrease of phosphorus concentration in bone. After thyroparathyroidectomy (Tx), the concentrations of inorganic phosporus and nitrogen diminished during some days, whereas the calcium content decreased continuously. Thyroxine application normalized the concentration of inorganic phosphorus. The osteolytic and nitrogen-anabolic effect of parathyroid hormone took place only in simultaneous treatment with thyroxine. The injection of calcitonin had a nitrogen-anabolic effect on bone; the simultaneous treatment with thyroxine induced a loss of calcium out of bone, and a deposition of calcium phosphate in renal tissue. Calcitonin did not inhibit a significant decrease of calcium concentration in the femur bone; the hypophosphatemic effect was always present. The metabolism of bone tissue, influenced by hormonal actions, probably determined the localization of the deposition of inorganic phosphorus, deserting the serum under the influence of calcitonin.

Animals↗
PubMed1979

[Regulation of calcium metabolism ; its rhythmic variations].

In rats fed a calcium-deficient diet, the amplitude of daily variation of plasma ionized and total calcium increased markedly whereas plasma 45Ca daily fluctuation remained essentially unchanged. Normal daily fluctuations in plasma 45Ca, lost after thyroparathyroidectomy, were restored by feeding rats a high-calcium diet. A suggestion is that circadian rhythmicity originates as a result of dynamic properties involving nonlinear processes of calcium metabolism.

Animals↗
PubMed1992

Parathyroid hormone inhibits 25-hydroxyvitamin D3-24-hydroxylase mRNA expression stimulated by 1 alpha,25-dihydroxyvitamin D3 in rat kidney but not in intestine.

Using a cDNA probe for rat renal 24-hydroxylase, expression of its mRNA was compared in the rat kidney and intestine. Vitamin D-deficient rats received a single injection of 1 alpha,25-dihydroxyvitamin D3. Expression of 24-hydroxylase mRNA was first detected in the kidney at 3-h post-injection and increased thereafter. Similarly, 24-hydroxylase mRNA was expressed in the intestine after 1 alpha,25-dihydroxyvitamin D3 injection. However, the dose level of 1 alpha,25-dihydroxyvitamin D3 required to induce the intestinal 24-hydroxylase mRNA expression was only 1/100 the amount required to induce renal 24-hydroxylase mRNA. Induction of intestinal 24-hydroxylase mRNA expression by 1 alpha,25-dihydroxyvitamin D3 was far more rapid than that of renal 24-hydroxylase mRNA. Thyroparathyroidectomy shortened the time required to induce expression of renal, but not intestinal, 24-hydroxylase mRNA. Administration of either parathyroid hormone or cAMP to vitamin D-deficient rats greatly reduced the expression of 24-hydroxylase mRNA in the kidney but not in the intestine. When rats were fed a vitamin D-repleted diet containing 0.7% (adequate) or 0.03% (low) calcium for 2 weeks, intestinal expression of 24-hydroxylase mRNA could be induced only in the low calcium group. In contrast, renal mRNA expression was preferentially stimulated in the adequate calcium group. These results clearly demonstrate that the expression of 24-hydroxylase mRNA is down-regulated by parathyroid hormone in the kidney but not in the intestine.

Animals↗