1,25-Dihydroxyvitamin D<sub>3</sub>Suppresses Parathyroid Hormone Secretion from Bovine Parathyroid Cells in Tissue Culture*

Cantley, Larry K.; Russell, John; Lettieri, Deborah; Sherwood, Louis M.

doi:10.1210/endo-117-5-2114

Cited by 228 publications

(80 citation statements)

References 20 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…According to the results shown in Fig. 1 Several studies suggest that 1 ,25(OH)2D3 directly inhibits the secretion of PTHfrom the parathyroid glands (22)(23)(24)(25) and also suppresses the production of PTHmRNA in parathyroid glands, independent of the concentration of ionized Ca (26)(27)(28). In the present study, the weekly administration of 8.0 |Ug of 1,25(OH)2D3 suppressed the PTH level without elevating the serum Ca.…”

Section: Discussionsupporting

confidence: 64%

Suppression of Secondary Hyperparathyroidism in Chronic Dialysis Patients by Single Oral Weekly Dose of 1,25-Dihydroxycholecalciferol.

et al. 1993

View full text Add to dashboard Cite

Eleven hemodialysis patients who developed refractory secondary hyperparathyroidism, despite conventional vitamin D therapy, were treated with large oral doses of 1,25-dihydroxycholecalciferol [1,25(OH)2D3]. Therapeutic regimen was a single oral dose of up to 8.0 jug administered once weekly following hemodialysis. A maximum serum level of 1,25(OH)2D occurred four hours after the 8.0 jig dose. A positive correlation (Y=84.3X-22.1: P<0.01) was found between the maximal serum 1,25(OH)2D concentration (Cmax) and the dose of 1,25(OH)2D3 when plotted on a logarithmic scale. Forty-eight hours after the administration of the 8.0 jag dose, the parathyroid hormone (PTH) level and the alkaline phosphatase activity (ALP) were markedly decreased without evidence of hypercalcemia. A significant inverse relationship was found between the Cmax of 1,25(OH)2D and the percent change in the PTH level measured after 48 hours, either with carboxy-terminal (C-PTH) or the highly sensitive mid-portion assay (HS-PTH). From these results, the level of serum 1,25(OH)2D required to blunt the rise in serum PTH was 168 pg/ml and 203 pg/ml, respectively; these serum levels were achieved by the oral administration of doses of 6.0-8.0 |LLg or higher. There were no adverse effects of treatment. Following this study, one patient was continuously treated with 8.0 jig of 1,25(OH)2D3 orally once a week for 18 months. There was a therapeutic effect (as evidenced by PTHsuppression, ALPsuppression and the disappearance of subjective complaints) without the development of severe hypercalcemia or hyperphosphatemia. This treatment may help to prevent or treat secondary hyperparathyroidism in patients receiving long-term dialysis.

show abstract

Section: Discussionsupporting

confidence: 64%

Suppression of Secondary Hyperparathyroidism in Chronic Dialysis Patients by Single Oral Weekly Dose of 1,25-Dihydroxycholecalciferol.

et al. 1993

View full text Add to dashboard Cite

show abstract

“…The regulation of PTH secretion involves several mediators, including extracellular calcium (Brown 1991), magnesium (Mayer & Hurst 1978), vitamin D (Cantley et al 1985) and, most recently, ET-1 (Eguchi et al 1992, Chang et al 1997. Parathyroid cells were reported to express the second most abundant ET-1 message in bovine species, and these cells secreted ET-1 into the culture medium (Fujii et al 1991).…”

Section: Discussionmentioning

confidence: 99%

In vivo effect of endothelin-1 on plasma calcium and parathyroid hormone concentrations

Sj²,

Tsai³

et al. 2000

Journal of Endocrinology

View full text Add to dashboard Cite

We have previously reported an in vitro inhibitory effect of endothelin-1 (ET-1) on parathyroid hormone (PTH) secretion. In the present experiment, ET-1 was infused into rabbits to study the in vivo effect of ET-1 on the changes in calcium, magnesium, PTH and calcitonin concentrations. Femoral arteries and veins of anesthetized male rabbits were cannulated to monitor vital signs, blood sampling and infusion of the agents being studied. Infusion of ET-1 (1, 5, 10 and 20 ng/kg per min) induced a dose-dependent decline in plasma ionized calcium concentrations from 6·68 0·26 to 5·50 0·46 mg/dl (P<0·05) and a decrease in calcitonin concentrations from 48·6 6·5 to 32·5 4·7 pg/ml. PTH concentrations increased from 58·3 10·2 to 159·4 22·1 pg/ml. In a separate experiment, calcium gluconate solution was simultaneously infused to keep calcium concentrations steady, thereby proving a calcium 'clamp'. In normal calcium concentration, ET-1 infusion gradually decreased PTH concentrations from 71·4 8·6 to 38·0 6·2 pg/ml. We further infused sodium citrate solution to decrease the calcium concentration (2·0 mg/dl less) and calcium gluconate solution was infused to keep calcium concentrations steadily less than normal. PTH concentrations were initially stimulated by the induction of hypocalcemia (68·1 11·2 to 135·6 8·5 pg/ml), but decreased by ET-1 infusion (135·6 8·5 to 85·1 15·2 pg/ml). Plasma magnesium concentrations did not change significantly throughout the entire study and calcitonin concentrations were not significantly changed during the calcium clamp studies. Serum phosphate and 1,25-(OH) 2 vitamin D 3 concentrations were also measured, but they also did not change significantly. In conclusion, ET-1 exhibited an in vivo acute hypocalcemic action, independent of calcitonin. It also directly decreased PTH secretion if serum calcium concentrations were kept steady. The above findings are consistent with the results of our previous in vitro experiment.

show abstract

“…[Ca ion ] may fall because increased phosphate will decrease the physicochemical driving forces for bone mineral dissolution (21) and favor ectopic precipitation of Ca phosphate complexes (90). In addition, phosphate retention will directly decrease serum 1,25(OH) 2 (99,(102)(103)(104)(105). In addition, during renal failure, there is decreased binding of 1,25(OH) 2 D 3 to the parathyroid cells (106).…”

Section: Ckd In Patients Who Are Not On Dialysismentioning

confidence: 99%

Contribution of Intestine, Bone, Kidney, and Dialysis to Extracellular Fluid Calcium Content

Bushinsky

2010

Clinical Journal of the American Society of Nephrology

View full text Add to dashboard Cite

Calcium (Ca) balance is the net of Ca intake and output from the body over a period of time. The concept of Ca balance does not consider the redistribution of Ca that often occurs in patients with chronic kidney disease (CKD), especially those who are on dialysis, which is often in the form of soft tissue and/or vascular calcification. In this article, we consider movement of Ca with respect to the extracellular fluid (ECF) and develop a mathematical formulation for Ca homeostasis with respect to the ECF that includes input and output from the diet, the bone, the kidney, and dialysis. We consider calcium homeostasis in healthy individuals and in patients with excess parathyroid hormone, excess 1,25-dihydroxyvitamin D 3 , and metabolic acidosis; patients who have CKD and are not on dialysis; and, finally, patients who have CKD and are on dialysis. On the basis of a number of assumptions, dialysis patients with a daily intake of >37.5 mmol of elemental Ca (1.5 g) have movement of Ca into the ECF even without supplemental activated vitamin D. Addition of activated vitamin D, which increases intestinal Ca absorption and can increase resorption of Ca from bone, leads to the movement of Ca into the ECF at virtually all levels of intake; however, there are numerous unanswered questions regarding Ca homeostasis in patients with CKD, including how much of the Ca, administered as a phosphate binder, is absorbed and what is the fate of this absorbed Ca. Until these pressing questions are answered with well-designed experiments, we do not know whether we are doing more harm than good for our dialysis patients by administering additional Ca as a phosphate binder, especially when they also receive activated vitamin D.

show abstract

1,25-Dihydroxyvitamin D₃Suppresses Parathyroid Hormone Secretion from Bovine Parathyroid Cells in Tissue Culture*

Cited by 228 publications

References 20 publications

Suppression of Secondary Hyperparathyroidism in Chronic Dialysis Patients by Single Oral Weekly Dose of 1,25-Dihydroxycholecalciferol.

Suppression of Secondary Hyperparathyroidism in Chronic Dialysis Patients by Single Oral Weekly Dose of 1,25-Dihydroxycholecalciferol.

In vivo effect of endothelin-1 on plasma calcium and parathyroid hormone concentrations

Contribution of Intestine, Bone, Kidney, and Dialysis to Extracellular Fluid Calcium Content

Contact Info

Product

Resources

About

1,25-Dihydroxyvitamin D3Suppresses Parathyroid Hormone Secretion from Bovine Parathyroid Cells in Tissue Culture*

Cited by 228 publications

References 20 publications

Suppression of Secondary Hyperparathyroidism in Chronic Dialysis Patients by Single Oral Weekly Dose of 1,25-Dihydroxycholecalciferol.

Suppression of Secondary Hyperparathyroidism in Chronic Dialysis Patients by Single Oral Weekly Dose of 1,25-Dihydroxycholecalciferol.

In vivo effect of endothelin-1 on plasma calcium and parathyroid hormone concentrations

Contribution of Intestine, Bone, Kidney, and Dialysis to Extracellular Fluid Calcium Content

Contact Info

Product

Resources

About

1,25-Dihydroxyvitamin D₃Suppresses Parathyroid Hormone Secretion from Bovine Parathyroid Cells in Tissue Culture*