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PubMed1989

Parathyroid hormone and calcitriol changes in normal and insulin-dependent diabetic pregnancies.

In pregnancy, an increase in serum calcitriol and parathyroid hormone concentrations has been reported in several studies, though the increase in parathyroid hormone remains controversial. In magnesium deficiency states, parathyroid hormone and calcitriol secretion may be decreased. Because magnesium deficiency may occur in insulin-dependent diabetic patients, mainly because of urinary magnesium losses, we hypothesized that serum parathyroid hormone and calcitriol do not increase in the diabetic pregnancy. We studied, in a prospective longitudinal manner, 35 nondiabetic and 199 insulin-dependent diabetic pregnancies. In diabetic women, the goals of glycemic control were fasting blood glucose below 100 mg/dL and postprandial blood glucose less than 140 mg/dL. Serum magnesium, calcium, parathyroid hormone (whole molecule; ie, 1-84 fragment), and calcitriol were measured three times: 1) 8-12 weeks, 2) 22-28 weeks, and 3) 32-38 weeks' gestation. In normal women, serum parathyroid hormone did not change significantly over pregnancy, and a wide scatter of values was observed. Serum calcitriol increased significantly with advancing gestation. In diabetic women, serum parathyroid hormone had a narrow scatter, but values were within the low-normal range. During the third trimester there was no increase, and even a decrease, in serum calcitriol concentrations. Diabetics had, throughout pregnancy, significantly reduced serum magnesium concentrations when compared with controls. Their serum calcium and ionized calcium concentrations were similar to those of controls, except in the third trimester, when diabetic women had significantly lower serum calcium and ionized calcium concentrations than controls. We speculate that mineral metabolism abnormalities in diabetic pregnancies might be due to relative magnesium and/or insulin deficiency.

Adult↗
PubMed1992

New actions of parathyroid hormone through its degradation.

Parathyroid hormone degradation is intimately connected with its action. By the action of the unique renal neutral cytosolic PTH ase, PTH is split into 1-34 and 35-84 fragments, and further into 35-70 and 71-84 fragments. Amino-terminal 1-34 peptide was found to participate in the autoregulation of PTH secretion, suppressing the intact PTH secretion both in vivo in humans and in vitro in the dispersed bovine parathyroid cells. C-terminal fragment 35-84 and N-terminal fragment 1-34 both suppress the alkaline phosphatase production by ROS 17/2.8 cells to a lesser extent than the intact PTH 1-84, and the sum of the effects of the two fragments approximately equaled that of the intact hormone. Fragments 35-70 and 71-84 were devoid of such activity. Intracellular free calcium of human vascular endothelial cells was raised by intact 1-84, lowered on the contrary by C-terminal 35-84 fragment, but fragments 1-34, 35-70 and 71-84 had no effect. Fragments generated by the actions, supporting the physiological significance of PTH degradation by its target cells.

Animals↗
PubMed1993

Stimulatory action of parathyroid hormone on renin secretion in vitro: a study using isolated rat kidney, isolated rabbit glomeruli and superfused dispersed rat juxtaglomerular cells.

1. We have previously reported that pharmacological concentrations (125nmol/l) of parathyroid hormone may stimulate renin release in the stable recirculating and non-filtering isolated rat kidney. 2. In the present study we have attempted to extend these initial observations by examining the concentration-related response of renin release to parathyroid hormone, using the same model of isolated kidney, and determining whether the effect of parathyroid hormone on renin release can be demonstrated by more direct approaches. Thus, the effects of parathyroid hormone on renin secretion were investigated in two other renal preparations: isolated rabbit glomeruli and isolated rat juxtaglomerular cells. 3. In the isolated kidney, rat parathyroid hormone significantly stimulated renin accumulation in the perfusate in a concentration-related manner with a threshold of 1 nmol/l. 4. In both glomeruli and juxtaglomerular cells bovine [Nle8,18,Tyr34]parathyroid hormone-(1-34)amide effectively and repeatedly stimulated renin release. These results imply that there is a direct stimulatory effect of parathyroid hormone on renin release. 5. We also examined the effect of [Nle8,18,Tyr34]parathyroid hormone-(1-34)amide during extracellular calcium buffering in the glomeruli. [Nle8,18,Tyr34]parathyroid hormone-(1-34)amide was uneffective in calcium-free medium. Increasing the extracellular ionized calcium concentration to 2.5 mmol/l increased the extent of stimulation in accordance with the reported ability of parathyroid hormone to block calcium channels and relax vascular smooth muscle cells. 6. These results provide further support for the role of parathyroid hormone as a direct mediator of renin secretion; moreover, the renin-stimulating action of parathyroid hormone may be mediated through the inhibition of calcium influx.

Animals↗
PubMed1992

Platelet cytosolic free calcium concentration and parathyroid hormone: changing relationships with haemodialysis in end-stage renal disease.

1. Twelve patients receiving haemodialysis for end-stage renal failure were studied at a single dialysis session. Platelet cytosolic calcium concentration, plasma ionized calcium concentration and serum parathyroid hormone concentration were measured before dialysis, mid-dialysis and 30 min after dialysis. 2. Plasma ionized calcium concentration increased towards dialysate calcium concentrations, falling insignificantly after cessation of dialysis. Serum parathyroid hormone concentration fell by 39% during dialysis, with incomplete recovery afterwards. There was no overall change in platelet cytosolic calcium concentration. 3. Patients were divided into two subgroups: low parathyroid hormone (serum parathyroid hormone concentration less than 10 pmol/l) and high parathyroid hormone (serum parathyroid hormone concentration greater than 10 pmol/l). Before dialysis, values of platelet cytosolic calcium concentration or plasma ionized calcium concentration were not statistically different between the subgroups, but the platelet cytosolic calcium concentration was higher in the high-parathyroid hormone subgroup during and after dialysis. 4. Before haemodialysis there was a linear correlation between plasma ionized calcium concentration and platelet cytosolic calcium concentration, which disappeared during dialysis. In contrast, there was no relationship between serum parathyroid hormone concentration and platelet cytosolic calcium concentration before dialysis, but after dialysis a hyperbolic relationship was evident. 5. These results suggest that uraemic toxins may interfere with cytosolic calcium homoeostasis, allowing passive diffusion of extracellular calcium to influence the resting concentration, and that this effect is reversible by haemodialysis.

Adult↗
PubMed1978

[Renal receptors of parathyroid hormone and calcitonin (author's transl)].

The two first steps of the renal cellular action of parathyroid hormone and of calcitonin are the hormonal binding onto specific receptors and the stimulation of adenylate cyclase by the hormone-receptor complex producing an increase in the intra-cellular concentration of 3'-5' cyclic adenosine monophosphate (cyclic AMP). Specific glomerular and tubular receptors for parathyroid hormone have been demonstrated using either tritiated parathyroid hormone or an indirect technique with 125 I labelled specific antibodies. Tubular receptors are localized both in the proximal and distal segments of the nephron. Parathyroid hormone stimulates glomerular and tubular adenylate cyclase. The main unsolved problem is the difficulty for demonstrating high affinity binding sites and stimulation of adenylate cyclase at low physiological concentrations of parathyroid hormone. In man, administration of parathyroid hormone produces a marked increase in the urinary excretion of cyclic AMP chiefly concerning its nephrogenous fraction. The peak of excretion is early and precedes the decrease in phosphate tubular reabsorption. Tubular receptors for calcitonin have been demonstrated using 125 I labelled salmon calcitonin. Calcitonin stimulates renal adenylate cyclase in only some segments of the nephron allowing receptors for calcitonin to be localized in the wide ascending branch of Henle's loop and the initial part of the convoluted distal tubule. In the presence of guanylnucleotides, binding of calcitonin onto its receptors and activation of adenylate cyclase are observed in the range of physiological concentrations of calcitonin in the rat. In man, administration of calcitonin produces a moderate increase in the urinary excretion of cyclic AMP coming from a non renal tissue.

Adenosine Monophosphate↗
PubMed1995

1,25 dihydroxyvitamin D and dexamethasone decrease in vivo Walker carcinoma growth, but not parathyroid hormone related protein secretion.

Parathyroid hormone related protein (PTHrP) is produced by several breast cancers. 1,25 dihydroxyvitamin D (1,25[OH]2D) and Dexamethasone (DEX) have been shown to decrease PTHrP mRNA expression in several cell lines. We therefore tested the in vivo effect of both steroids on PTHrP secretion and tumor development of the Walker carcinoma (WC). WC cells were injected subcutaneously in Fisher rats which were simultaneously treated with either vehicle, or 1,25(OH)2D (0.5 micrograms/kg/d) or DEX (2 mg/kg/d). After 7 days, tumor weight was significantly decreased in the 2 treated-groups as compared to the control group. Vehicle treated-rats developed hypercalcemia, which was also observed in rats treated with 1,25(OH)2D; by contrast, the plasma calcium was significantly decreased in the DEX-treated group compared to vehicle-treated rats. In a dose-effect experiment, this dose of 1,25(OH)2D induced marked hypercalcemia in rats not implanted with WC, but was required to decrease the tumor weight in implanted rats. In both 1,25(OH)2D and DEX-treated groups, plasma PTHrP levels were significantly decreased, but there was a similar correlation between PTHrP plasma level and tumor weight in the three groups. Indeed, the cytosolic PTHrP content/mg tumor was identical in the 3 groups. By contrast, the PTHrP/Actin mRNA in the tumor was significantly decreased in the 1,25(OH)2D group, comparatively to the vehicle and DEX groups. Our results show that Dexamethasone and 1,25(OH)2D decrease WC tumor development in vivo, but do not change the PTHrP secretion by the remaining tumor although steady state PTHrP mRNA content level is decreased by 1,25(OH)2D.

Animals↗
PubMed1992

Regulation of acute parathyroid hormone release in normal humans: combined calcium and citrate clamp study.

The objective of the present study was to elucidate the dynamics of parathyroid hormone regulation, with particular reference to the mechanism controlling the acute parathyroid hormone release. Through utilization of the citrate clamp technique and the calcium clamp technique we were able, in a standardized way, to stimulate and suppress the parathyroid hormone secretion. Precise bedside measurements of blood ionized calcium and measurements of intact parathyroid hormone were performed. Twelve healthy young volunteers participated in two trials 6-12 wk apart, a citrate clamp (delta-blood ionized calcium -0.19 mmol/l) and a calcium plus citrate clamp (delta-blood ionized calcium +0.22 mmol/l and -0.19 mmol/l). During the citrate clamp, preceded by normal calcemia, serum intact parathyroid hormone peaked to a maximum after 5-10 min, four to six times above baseline concentration and then declined to a steady state two to three times above baseline concentration. During the citrate clamp, preceded by hypercalcemia induced by a calcium clamp, serum intact parathyroid hormone also peaked immediately to about five to nine times above its suppressed level, approximately two times above the baseline concentration. Subsequently, serum intact parathyroid hormone declined to a steady state just below the baseline concentration. In conclusion, within the range studied, the mechanism eliciting the acute serum intact parathyroid hormone release from its depot is a fall in blood ionized calcium, not the absolute concentration of ionized calcium.

Adult↗
PubMed2005

Ex vivo expansion of hemopoietic precursor cells on a sublayer treated with parathyroid hormone.

The kinetics of hemopoietic precursor cells was studied in cultures treated with parathyroid hormone in a concentration of 10(-7) M. Long-term culturing of bone marrow with parathyroid hormone did not change the number of mature cells, while the number of precursors forming colonies in semisolid media increased 7-fold and the number of cells forming cobblestone areas on day 28 increased 9-10-fold. After 24 h culturing of bone marrow cells on an irradiated sublayer pretreated with parathyroid hormone for 8 and 12 weeks, the number of early hemopoietic precursor cells forming cobblestone areas on day 28 of culturing increased 2-and 5.5-fold, respectively. The expression of Bmi-1 gene responsible for self-maintenance of stem hemopoietic cells increased in cultures treated with parathyroid hormone. It seems that parathyroid hormone can be used for expansion of hemopoietic stem cells ex vivo, which is essential for their transplantation to patients.

Animals↗
PubMed1990

[Secretion of thyrocalcitonin and parathyroid hormone in diffuse polyposis of the colon].

The article presents data obtained in studying the content of calcium regulating hormone thyrocalcitonin and parathyroid hormone in blood plasma of patients with diffuse polyposis of the colon prior to and after a radical surgical treatment. The content of these hormones was also studied in extracts from colonic polyps. The concentration The concentration of thyrocalcitonin was found to decrease after operation. The elevated concentration of thyrocalcitonin was established in polyp extracts which might suggest its "ectopic secretion" in the polyp tissue in diffuse polyposis. Removal of the colon with polyps is followed by normalization of metabolism in the organism which proves the expediency of early surgical treatment.

Adenomatous Polyposis Coli↗
PubMed1981

Parathyroid hormone inhibition of phosphate transport in renal brush border vesicles from phosphate-depleted dogs.

Dietary phosphate (Pi) restriction increases renal Pi reabsorption and induces resistance to the phosphaturic action of parathyroid hormone. Na+-gradient-stimulated Pi transport in membrane vesicles isolated from the renal brush border of experimental animals has been shown to parallel changes in renal Pi reabsorption induced by dietary Pi restriction and in vivo administration of parathyroid hormone. Dietary Pi restriction has been shown to markedly inhibit the phosphaturic response to parathyroid hormone in rats and dogs. Parathyroid hormone has been reported not to decrease the Na+-gradient-stimulated transport of Pi in brush border membrane vesicles isolated from dietary Pi restricted rats unless the rats were administered an acute Pi load prior to killing, however, thyroparathyroidectomy of rats fed a low Pi diet has been reported to increase Na+-gradient-stimulated Pi transport. Using the dietary Pi restricted dog, we demonstrated no significant decrease in renal reabsorption of Pi in response to parathyroid hormone administration. However, significant decreases in Pi transport in brush border membrane vesicles isolated from the kidneys of dietary Pi restricted dogs were observed in response to in vivo parathyroid hormone administration. These data demonstrate that the resistance to the phosphaturic action of parathyroid hormone observed in vivo does not include resistance to the inhibitory effect of parathyroid hormone on Pi transport in brush border membrane vesicles. Thus, the data suggest that parathyroid hormone continues to alter Pi transport characteristics of the brush border membrane in states of Pi depletion despite the resistance to parathyroid hormone seen in vivo.

Animals↗
PubMed1984

Parathyroid hormone receptors in circulating human mononuclear leukocytes.

In this article we demonstrate receptors for parathyroid hormone in circulating mononuclear leukocytes using the radioiodinated analogue (8,18 norleucine, 34 tyrosine) bPTH 1-34 (bovine parathyroid hormone 1-34). Specific binding, which is reversible and saturable, equilibrates within 5 min at 0-4 degrees C with a calculated KD of 8.9 X 10(-11) M. This binding has a pH maximum of 7.0, is magnesium-dependent, and is inversely related to medium calcium concentration. Such binding is completely inhibited by simultaneous addition of 4 ng/ml of bovine parathyroid hormone 1-34, 5 ng/ml of bovine parathyroid hormone 1-84, or 5 ng/ml (8,18 norleucine, 34 Tyr) of 3-34 bPTH, but is unaffected by a biologically inactive parathyroid hormone fragment or other unrelated peptide hormones. Cyclic AMP accumulation increases 3-fold after 5 min exposure of mononuclear leukocytes to bPTH 1-34 in concentrations as low as 1 X 10(-9) M. Lymphocytes appear to be the circulating cells which interact with PTH as indicated by the observations that: 1) lymphocyte-enriched preparations bind three times as much radioligand/cell as do mixed mononuclear leukocytes, 2) monocytes, platelets, granulocytes, and erythrocytes do not bind PTH, and 3) monocytes, but not lymphocytes, degrade the hormone.

Cell Separation↗
PubMed2000

Hormonal regulation of [Ca(2+)](i) in periosteal-derived osteoblasts: effects of parathyroid hormone, 1,25(OH)(2)D(3) and prostaglandin E(2).

The effects of hormonal modulators of osteoblast function, parathyroid hormone, 1,25(OH)(2)D(3) and prostaglandins on [Ca(2+)](i) in periosteal-derived osteoblasts from rat femurs have been investigated. Our results show that application of parathyroid hormone PTH (10(-5) M) and prostaglandin E(2) (PGE(2)) (4 microM) result in a rapid heterogeneous elevation in [Ca(2+)](i) that, in the case of PTH, is dependent on both extracellular and intracellular sources of calcium. Variable responses to treatments have been found within populations of cells. The PGE(2) response is dose dependent. Treatment with 1,25(OH)(2)D(3) (10(-8) M) induces a brief (60-90 sec) elevation in [Ca(2+)](i) that is almost totally abolished in EGTA-buffered Ca(2+)-free medium. Interactive effects of multiple hormone treatments have been observed. Pretreatment with 1,25(OH)(2)D(3) results in near-total inhibition of the PTH and PGE(2) responses. In conclusion, modulation of [Ca(2+)](i) appears to play a role not only in the direct effects of osteotropic hormones on osteoblasts but also in the synergistic and antagonistic effects between circulating hormones.

Aniline Compounds↗
PubMed1997

Mitochondrial membrane potential changes in osteoblasts treated with parathyroid hormone and estradiol.

This study assessed mitochondrial membrane potential changes in cultured osteoblasts treated with hormones known to regulate osteoblasts. A fluorescent carbocyanine dye, 5,5',6,6'-tetrachloro-1,1',3,3'-tetraethylbenzimidazolocarbocyanine++ + iodide, also called JC-1, was used as a probe. JC-1 emits photons at 585 nm (orange-red) when the membrane potential in mitochondria is highly negative, but when the potential becomes reduced emission occurs at 527 nm (green). Osteoblasts were rinsed in serum-free medium for 5 min, then loaded with 1 x 10(-6) M JC-1 for 10 min. The distribution and intensity of JC-1 fluorescence were evaluated with a laser-scanning confocal microscope system. Hormone treatments included parathyroid hormone (PTH; 10(-8) M), 17beta-estradiol (10(-8) M), and thyroxine (T4; 10(-8) M). The potassium ionophore valinomycin (10(-6) M) was used as a control since it is known to disrupt the electrochemical gradient of mitochondria without interfering with the pH gradient. Valinomycin caused a profound, rapid increase (22.5% above untreated values) in the green/red ratio, which indicated a lowering of the mitochondrial membrane potential in all samples evaluated. PTH caused a less pronounced, but significant (7-14%), reduction in membrane potential in all cells examined. PTH is known to affect osteoblasts in a number of ways and is inhibitory to mitochondrial respiration; the results confirm this effect. For estradiol, half of the cells responded at a significant level, with a membrane potential reduction of 6 to 13% being recorded; the other half did not respond. Thyroxine did not alter mitochondrial membrane potential. Responses were detectable within 20 s for valinomycin, but occurred at a slower rate, over 200 to 300 s, following PTH and estradiol treatment. Responses to PTH and estradiol could be due to mitochondrial uptake of cytosolic Ca2+.

Animals↗
PubMed1990

Effect of propranolol on phosphate reabsorption by superficial nephron segments in response to parathyroid hormone in phosphate-deprived rats.

Phosphate deprivation causes a resistance to the phosphaturic effect of parathyroid hormone. The decreased phosphaturic response to parathyroid hormone in rats fed a low phosphate diet for 1 day can be restored by propranolol infusion. Free-flow micropuncture studies were performed to localize the nephron site of restoration of the phosphaturic effect of parathyroid hormone by propranolol in rats deprived of phosphate for one day. In animals fed low phosphate diet and in the presence of parathyroid hormone, propranolol infusion did not change phosphate delivery to the late proximal tubule; however, fractional delivery of phosphate to the early distal tubule was significantly increased from 18.3 +/- 2.9 to 32.2 +/- 4.1%. In rats fed a normal phosphate diet, propranolol infusion did not change phosphate delivery along the nephron. We conclude that the restoration of the phosphaturic effect of parathyroid hormone by propranolol infusion in rats deprived of phosphate for 1 day is primarily due to decreased reabsorption of phosphate by superficial loop segments, most likely the pars recta segment of the proximal tubule.

Absorption↗
PubMed1985

Calcium, parathyroid hormone, and hypertension.

Both calcium and parathyroid hormone appear to be involved in the acute and chronic regulation of arterial pressure in experimental animals and humans. While the direct evidence is still preliminary, the net effect of calcium and parathyroid hormone under normal physiologic conditions is to favor a reduction in blood pressure. The implications of this assessment for common medical disorders, such as essential hypertension, and less common but oftentimes more challenging clinical conditions, such as end-stage renal disease, are potentially substantial.

Animals↗
PubMed1977

Control of parathyroid hormone hydrolysis by the kidney.

In order to assess the role of the kidney in controlling the degradation, fate, half-life, and consequently the functional level of the parathyroid hormone in vivo, highly purified bovine parathyroid hormone (bPTH 1-84) and synthetic N-terminal peptide of the bovine parathyroid hormone (bPTH 1-34) were iodinated and their hydrolysis by the kidney and liver tissue of rats were measured under various levels of parathyroid function and calcium metabolism. While the hydrolysis of bPTH 1-84 did not change significantly in response to acute change of serum parathyroid hormone in response to injections of EDTA, phosphate, and calcium or after parathyroidectomy, less bPTH 1-34 was hydrolyzed 60 min after injection of EDTA or phosphate along with the rise of serum PTH than in the controls. No significant change was found in the hydrolysis of bPTH 1-34 after calcium infusion or parathyroidectomy with a consequent fall of serum parathyroid hormone. Increase of calcium ions in the incubation medium in vitro resulted in a more pronounced increase of bPTH 1-34 hydrolysis than that of bPTH 1-84. Hydrolysis of the N-terminal portion of parathyroid hormone probably plays a more important role in the acute control of the functional level of the parathyroid hormone than the hydrolysis of the whole molecule.

Animals↗