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PubMedDate not supplied

The effect of thyroparathyroidectomy: development of disuse osteoporosis in adult rats.

The present investigation was undertaken in order to study the role played by the thyroid and the parathyroid glands in the development of osteoporosis induced by immobilization. One hundred and fifty-three male adult Sprague-Dawley rats were divided into 2 groups. The animals of one group were thyroparathyroidectomized; those of the other group were left intact. Each group was then divided into two subgroups in one of which the right hind leg of the animals were immobilized by elastic adhesive bandages. The animals were observed for varying periods of time up to 16 weeks. Bone mass and composition was determined and the results indicated that disuse osteoporosis occurs in rats in the virtual absence of the thyroid and parathyroid glands. The bone loss of the immobilized femur and tibia is however less pronounced in thyroparathyroidectomized than in intact rats.

Animals↗
PubMed1977

The hypocalcemic activity of pancreatic tissue homogenate in the dog.

Glucagon and the pancreatic homogenate preparations to be tested for hypocalcemic effects were injected either intravenously or intraperitoneally in thyroparathyroid intact dogs and in dogs after thyroparathyroidectomy, respectively. Evidence has been presented that, in thyroparathyroid intact dogs, pancreatic tissue homogenate and the residue of such homogenate demonstrated a maximal hypocalcemic effect and that, in the thyroparathyroid intact dog, glucagon produced a hypocalcemic effect but did not produce a significant effect on dogs after acute thyroparathyroidectomy. On the other hand, the hypocalcemic effect of residue was equally effective both in dogs after thyroparathyroidectomy and in thyroparathyroid intact dogs; there was evidence that intravenous infusion of the residue resulted in a more rapid decrease in serum calcium levels compared with the intraperitoneal infusion after thyroparathyroidectomy of dogs being maintained four to five days with parathormone. Although final conclusions are not justifiable, the results suggest that a pancreatic factor other than glucagon has hypocalcemic effects and might explain the hypocalcemia observed during acute pancreatitis.

Animals↗
PubMed1984

Thyroid replacement in thyroparathyroidectomized dogs.

The thyroparathyroidectomized dog is an important experimental model of hypoparathyroidism and has been widely utilized for acute and chronic studies of the physiologic role of parathyroid hormone on systemic and renal acid-base, electrolyte and vitamin D physiology. Despite widespread use of this model, the appropriate thyroid hormone replacement dose necessary for achievement of postoperative euthyroidism has not been established for this species. Accordingly, serum thyroxine (T4) concentration was measured prior to and following chronic thyroparathyroidectomy in dogs given thyroid hormone replacement at different doses and routes of administration: sodium levothyroxine, 2.4 micrograms/kg daily in one or two divided subcutaneous doses (group I, n = 9), 20 micrograms/kg daily in two divided oral doses (group II, n = 8), and a wide range of intravenous doses (group III, n = 3). Group I dosage was based on the reported T4 production rate in dogs and is slightly greater than the reported production rate in man. Group II dosage was based on published clinically derived estimates of required replacement amounts. With subcutaneous replacement (group I) serum T4 concentration decreased from a preoperative value of 1.80 +/- 0.20 to 0.60 +/- 0.10 microgram/100 ml (p less than 0.001) following thyroparathyroidectomy. With oral replacement (group II), serum T4 concentration after thyroparathyroidectomy was not significantly changed from control (1.88 +/- 0.22 vs. 1.66 +/- 0.43 microgram/100 ml). Group III studies revealed that both total and free serum T4 concentration could be normalized after thyroparathyroidectomy with an intravenous dose of 10 micrograms/kg daily. As found with subcutaneous administration, intravenous replacement with lesser amounts of T4 than 10 micrograms/kg daily (i.e. 2.5 micrograms/kg) resulted in significant decreases in serum T4 concentration from control.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1980

Regulation of canine renal vesicle Pi transport by growth hormone and parathyroid hormone.

Renal phosphate (Pi) reabsorption is increased by growth hormone (GH) and decreased by parathyroid hormone (PTH). Na+-stimulated Pi transport across the brush border membrane of the proximal tubule is the initial step in the process of Pi reabsorption. To determine whether changes in Pi reabsorption induced by GH or PTH are accompanied by changes in brush border membrane Na+-gradient-stimulated Pi transport, we examined the effect of in vivo GH and PTH administration and thyroparathyroidectomy on Pi transport by isolated brush border membrane vesicles prepared from canine kidney. In experiments in which the effect of PTH administration was examined, the same animal provided the control kidney (before PTH administration) and the experimental kidney (after PTH administration). The Na+-gradient Pi overshoot in vesicles isolated from normal, GH-treated and thyroparathyroidectomized dogs was increased after in vivo PTH administration. GH administration and thyroparathyroidectomy increased the height of the overshoot compared to normal. PTH administration decreased the apparent V value by 44% in vesicles from normal animals. The apparent V value was increased, compared to normal, by GH (34%) and thyroparathyroidectomy (57%). PTH administration decreased the apparent V in both the latter groups. GH administration to thyroparathyroidectomized dogs further increased the apparent V. Changes in the apparent V paralleled changes in Pi reabsorption in vivo induced by experimental manipulations. We conclude that changes in renal Pi reabsorption induced by GH were like those induced by PTH, accompanied by changes in the Na+-stimulated Pi transport system in the renal brush border membrane, and that the effect of PTH on vesicular Pi transport in GH-treated dogs did not differ from the effect on vesicles from normal animals.

Animals↗
PubMed1991

Effect of aluminium on urinary acidification in the rat: influence of parathyroid hormone.

1. The influence of thyroparathyroidectomy and/or acidosis on renal function and specifically on acid excretion was studied in rats treated with a cumulative dose of 2 mg of aluminium. 2. Aluminium-treated and non-treated thyroparathyroidectomized rats showed a significant decrease in glomerular filtration rate and in the urinary/plasma inulin ratio without alteration in net acid excretion. 3. Non-treated thyroparathyroidectomized acidotic rats showed a significant fall in the amount of ammonium excreted and in overall acid excretion, suggesting that parathyroid hormone participates in an important way in the defence against metabolic acidosis. 4. The effects of acidosis, thyroparathyroidectomy and aluminium treatment on renal function parameters were not additive, suggesting a common final mechanism. In normal or acidotic aluminium-treated rats, thyroparathyroidectomy had no effect on renal acid excretion, suggesting that aluminium even in low doses inhibited the action of PTH on the renal tubule. 5. After exposure to aluminium, the relative inhibition of PTH on the renal tubule may become an additional factor that could contribute to the worsening of clinical conditions in which an inappropriate retention of acid loads can occur.

Acidosis↗
PubMed1988

Renal response to parathyroid hormone in the weanling rat.

The renal response to parathyroid hormone and the activity of alkaline phosphatase in kidney cortex were studied in weanling and adult rats. Clearance studies for the determination of glomerular filtration rate and phosphate excretion were started 2 h after sham operation or thyroparathyroidectomy in 24- or 40-day-old rats. Urine was collected under basal conditions and following infusions with 0.5 and 1.0 mumol phosphate per 100 g body wt min-1. For enzyme studies, rats aged 14-40 days were used, and the activity of alkaline phosphatase in renal cortical slices was determined. Glomerular filtration rate was not influenced by thyroparathyroidectomy or phosphate infusions. Plasma phosphate increased during phosphate infusions and was significantly higher in thyroparathyroidectomized rats in all clearance periods. Both the net and the fractional excretions of phosphate were higher in intact than in thyroparathyroidectomized rats and the phosphate-retaining effect of thyroparathyroidectomy was similar in weanling and adult rats. Alkaline phosphatase activity in renal cortical slices increased between days 14 and 24 (1400-3190 IU mg-1 protein, P less than 0.01). During later development, no significant change was seen. It is concluded that the immature kidney of the weanling rats shows a parathyroid hormone-dependent adaptation to acute phosphate loading, and that changes in alkaline phosphatase activity are consistent with a maturation of this system only during early development.

Alkaline Phosphatase↗
PubMed1980

Comparison of the regulation of calcitonin in serum of old and young Buffalo rats.

Studies were carried out to characterize the secretion and the effects of calcitonin in the Buffalo rat. Mean basal concentrations of calcitonin and parathyroid hormone were significantly increased in serum of rats older than 6 months of age as compared with rats between 2 and 3 months of age. The mean concentration of calcium in serum was independent of age. In both age groups, serum calcitonin was increased by administration of calcium (1 mmol/kg body wt) or isoproterenol (100 microgram/kg body wt), was diminished by beta-adrenergic blockade with DL-propranolol (1 mg/kg body wt) and was not altered by either pentagastrin or glucagon (200 and 100 microgram/kg body wt respectively). The average weight of the thyroid glands was significantly greater in the old than in the young animals but the mean concentration of calcitonin in the thyroids was the same. Thyroparathyroidectomy produced a transient increase followed by a fall in mean serum calcium in the old rats. In contrast, a progressive decline in the mean concentration of calcium in serum was observed after thyroparathyroidectomy in the young rats. Treatment of old animals with reserpine (2.5 mg/kg body wt) markedly depleted noradrenaline in the thyroid, lowered calcitonin in serum and converted the pattern of response of serum calcium to thyroparathyroidectomy to that observed in young animals. The results provide evidence that hypercalcitonaemia occurs in aged Buffalo rats, as does hyperparathyroidism, and that the concentrations of calcitonin in blood are modulated by beta-adrenergic affectors. Glucagon and pentagastrin exhibit little if any effects on calcitonin secretion in this strain of rat regardless of age.

Aging↗
PubMed1991

Functional analysis of ectopic parathyroid activity in cats.

The ability of ectopic parathyroid tissue to support calcium homeostasis was evaluated by measuring serum concentrations of calcium, phosphorus, albumin, magnesium, and parathyroid hormone before and for 12 weeks after bilateral thyroparathyroidectomy in 14 cats. During the immediate postoperative period, significant decrease was observed in serum calcium, magnesium, and parathyroid hormone (PTH) concentrations. Serum PTH concentration remained subnormal and did not significantly increase during the 12-week observation period. Despite persistent hypoparathyroidism, serum calcium and magnesium concentrations gradually increased. Ectopic parathyroid tissue is not capable of maintaining normal serum calcium concentration immediately after thyroparathyroidectomy. Serum calcium concentration gradually normalizes after thyroparathyroidectomy, apparently by means of a PTH-independent mechanism.

Animals↗
PubMed1992

Ca2+ uptake by endoplasmic reticulum of renal cortex. II. Effects of uninephrectomy and parathyroidectomy.

Calcium uptake by the endoplasmic reticulum (ER) is important for cellular calcium homeostasis, yet its regulation in nonmuscle cells is poorly understood. We reported that Ca2+ uptake by a light fraction of canine renal cortical ER (LER) is stimulated by protein kinase C in vitro. Here we describe conditions in vivo that stimulate renal cortical LER Ca2+ uptake. Thirty minutes after contralateral nephrectomy in the dog, 45Ca2+ uptake into renal cortical LER was increased 42% above control LER. There was no difference in LER Ca2+ uptake 24 hours after uninephrectomy. Acute denervation did not reproduce the increase in LER 45Ca2+ uptake seen at 30 minutes after uninephrectomy, nor did prior thyroparathyroidectomy abolish it. Forty-eight hours after thyroparathyroidectomy, 45Ca2+ uptake activity into renal cortical LER was decreased approximately sevenfold. In a proximal tubular cell line (LLC-PK1), 30-minute incubation with 12-O-tetradecanoylphorbol-13-acetate doubled 45Ca2+ uptake into a nonmitochondrial pool. Pretreatment with epidermal growth factor halved ER Ca2+ uptake, whereas insulin-like growth factor and growth hormone, alone or in combination, had no effect. Our data suggest that Ca2+ uptake into renal cortical ER is stimulated acutely during compensatory renal growth, perhaps through protein kinase C, and is stimulated chronically by parathyroid hormone.

Animals↗
PubMed1982

Abnormal skeletal response to parathyroid hormone in dogs with chronic uremia.

The release of cyclic AMP from bone in response to stimulation with PTH 1-34 was examined in 20 dogs with long-term chronic renal failure (CRF) produced by unilateral nephrectomy and contralateral partial renal artery ligation. After 9 to 15 months of uremia, the tibiae were removed and perfused in vitro. Seven dogs with CRF served as controls, 7 dogs with CRF were treated with 24,25(OH)2D3 - 2.5 micrograms per day, and 6 CRF dogs underwent thyroparathyroidectomy (TPTX) 42 h before they were sacrificed. The release of cyclic AMP from bone in response to PTH 1-34 in the CRF dogs was severely reduced compared to the response observed in 7 dogs with normal renal function (net accumulation of cyclic AMP release 86 +/- 8.5 versus 426 +/- 59.0 pmol/30 min). Long-term treatment of uremic dogs with 24,25(OH)2D3 had no effect on the release of cyclic AMP by bone. However, the release of cyclic AMP was restored to normal levels in the CRF dogs that underwent thyroparathyroidectomy. All CRF dogs had secondary hyperparathyroidism and the fact that TPTX returned the cyclic AMP response to normal values suggests that desensitization to PTH of the adenylate cyclase system of bone exists in chronic uremia.

24,25-Dihydroxyvitamin D 3↗
PubMed1982

Role of parathyroid hormone and 1,25-dihydroxyvitamin D3 in the development of osteopenia in oophorectomized rats.

The effect of ovarian insufficiency on calcium metabolism has been thought to involve an increased bone resorptive effect of parathyroid hormone and possible impaired synthesis of 1,25-dihydroxyvitamin D3. In the present study a rat model allowing for controlled serum levels of parathyroid hormone and 1,25-dihydroxyvitamin D3 was used. Oophorectomy in this species is associated with increased serum levels of 1,25-dihydroxyvitamin D3 and decreased bone mass. Although thyroparathyroidectomy increased bone mass, an increased sensitivity of bone to parathyroid hormone in oophorectomized rats was not observed. Thus the development of the osteopenia did not seem to be related to increased parathyroid hormone sensitivity or to reduced levels of 1,25-dihydroxyvitamin D3. Exogenous 1,25-dihydroxyvitamin D3 increased bone mass in oophorectomized as well as intact rats. Intestinal calcium transport was increased by moderate doses of 1,25-dihydroxyvitamin D3. Intestinal calcium transport was also reduced by thyroparathyroidectomy and increased by the administration of parathyroid extract. A tendency for increased accumulation of 1,25-dihydroxyvitamin D3 in blood in oophorectomized rats has been noted. It is suggested that the tendency to hypercalcemia in ovarian-insufficient females given 1-hydroxylated vitamin D compounds may be related to a diminished metabolism of 1,25-dihydroxyvitamin D3.

Animals↗