scholarly journals Correction of acidosis in hemodialysis patients increases the sensitivity of the parathyroid glands to calcium.

1997 ◽  
Vol 8 (4) ◽  
pp. 627-631
Author(s):  
K A Graham ◽  
N A Hoenich ◽  
M Tarbit ◽  
M K Ward ◽  
T H Goodship
Keyword(s):  
Parathyroid Hormone ◽  
Dynamic Assessment ◽  
Hormone Secretion ◽  
Hemodialysis Patients ◽  
Parathyroid Glands ◽  
Ionized Calcium ◽  
Optimal Correction ◽  
Blood Ph ◽  
Parathyroid Function ◽  
Before And After

Correction of acidosis in hemodialysis patients increases the sensitivity of the parathyroid glands to calcium. In this study, the parathyroid response to the correction of acidosis in eight hemodialysis patients was determined by performing dynamic assessment of parathyroid function before and after the correction of acidosis. The parathyroid response to intravenous calcitriol before and after the correction of acidosis was also assessed. After optimal correction of acidosis, there were no significant changes in blood pH, ionized calcium, phosphate, or alkaline phosphatase values, but the level of venous total CO2 increased significantly. Parathyroid hormone/ionized calcium curves were displaced downward after correction of acidosis, but not after the administration of intravenous calcitriol. The correction of metabolic acidosis in hemodialysis patients with secondary hyperparathyroidism can suppress parathyroid hormone secretion by increasing the sensitivity of the parathyroid glands to ionized calcium.

scholarly journals Relationship between parathyroid calcium-sensing receptor expression and potency of the calcimimetic, cinacalcet, in suppressing parathyroid hormone secretion in an in vivo murine model of primary hyperparathyroidism

2005 ◽  
Vol 153 (4) ◽  
pp. 587-594 ◽  
Author(s):  
Takehisa Kawata ◽  
Yasuo Imanishi ◽  
Keisuke Kobayashi ◽  
Takao Kenko ◽  
Michihito Wada ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Primary Hyperparathyroidism ◽  
Secondary Hyperparathyroidism ◽  
Murine Model ◽  
Hormone Secretion ◽  
Suppressive Effect ◽  
Receptor Expression ◽  
Parathyroid Glands ◽  
Calcium Sensing Receptor ◽  
Calcium Sensing

Cinacalcet HCl, an allosteric modulator of the calcium-sensing receptor (CaR), has recently been approved for the treatment of secondary hyperparathyroidism in patients with chronic kidney disease on dialysis, due to its suppressive effect on parathyroid hormone (PTH) secretion. Although cinacalcet’s effects in patients with primary and secondary hyperparathyroidism have been reported, the crucial relationship between the effect of calcimimetics and CaR expression on the parathyroid glands requires better understanding. To investigate its suppressive effect on PTH secretion in primary hyperparathyroidism, in which hypercalcemia may already have stimulated considerable CaR activity, we investigated the effect of cinacalcet HCl on PTH-cyclin D1 transgenic mice (PC2 mice), a model of primary hyperparathyroidism with hypo-expression of CaR on their parathyroid glands. A single administration of 30 mg/kg body weight (BW) of cinacalcet HCl significantly suppressed serum calcium (Ca) levels 2 h after administration in 65- to 85-week-old PC2 mice with chronic biochemical hyperparathyroidism. The percentage reduction in serum PTH was significantly correlated with CaR hypo-expression in the parathyroid glands. In older PC2 mice (93–99 weeks old) with advanced hyperparathyroidism, serum Ca and PTH levels were not suppressed by 30 mg cinacalcet HCl/kg. However, serum Ca and PTH levels were significantly suppressed by 100 mg/kg of cinacalcet HCl, suggesting that higher doses of this compound could overcome severe hyperparathyroidism. To conclude, cinacalcet HCl demonstrated potency in a murine model of primary hyperparathyroidism in spite of any presumed endogenous CaR activation by hypercalcemia and hypo-expression of CaR in the parathyroid glands.

scholarly journals Parathyroid hormone-producing cells exist in adipose tissues surrounding the parathyroid glands in hemodialysis patients with secondary hyperparathyroidism

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Takatoshi Kakuta ◽  
Kaichiro Sawada ◽  
Genta Kanai ◽  
Ryoko Tatsumi ◽  
Takayo Miyakogawa ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Secondary Hyperparathyroidism ◽  
Hemodialysis Patients ◽  
Parathyroid Glands ◽  
Adipose Tissues

THE EFFECTS OF CALCITONIN AND PARATHORMONE ON PLASMA MAGNESIUM LEVELS BEFORE AND AFTER BIRTH IN THE RAT

1974 ◽  
Vol 61 (1) ◽  
pp. 1-13 ◽  
Author(s):  
J. M. GAREL ◽  
J. P. BARLET
Keyword(s):  
Parathyroid Hormone ◽  
Salmon Calcitonin ◽  
Magnesium Level ◽  
Plasma Calcium ◽  
Parathyroid Glands ◽  
Small Decrease ◽  
Newborn Rats ◽  
Newborn Rat ◽  
Before And After ◽  
Plasma Magnesium

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.

Prolactin stimulation of parathyroid hormone secretion in bovine parathyroid cells

1984 ◽  
Vol 247 (5) ◽  
pp. E675-E680 ◽  
Author(s):  
L. Magliola ◽  
L. R. Forte
Keyword(s):  
Parathyroid Hormone ◽  
Hormone Secretion ◽  
Vitamin D Metabolism ◽  
Parathyroid Function ◽  
Wide Range ◽  
Camp Levels ◽  
Bovine Species ◽  
Ca Homeostasis

Previous studies have suggested that prolactin (PRL) may affect calcium (Ca) homeostasis by an action on vitamin D metabolism. In this study, the effects of PRL on parathyroid hormone (PTH) secretion were investigated in dispersed bovine parathyroid cells (PTC). PRL (0.013-1.3 microM) caused concentration-dependent increases in PTH secretion. PRL-stimulated PTH release was apparent as early as 1 h and was progressive thereafter for up to 3 h. PRL enhanced PTH release over a wide range of ambient Ca concentrations (0.5-2.0 microM). Ovine and rat PRL were more effective than bovine PRL in stimulating PTH secretion. This effect was apparently specific for PRL because neither ovine nor bovine growth hormone stimulated PTH secretion. PRL-stimulated PTH release was not mediated through the beta-adrenergic or dopaminergic receptor systems of PTC and was not associated with increased adenosine 3',5'-cyclic monophosphate (cAMP) levels. This study demonstrated a direct effect of PRL to stimulate PTH secretion in vitro. Although these data do not provide evidence for an effect of PRL in vivo, we suggest a mechanism by which PRL may influence parathyroid function and Ca homeostasis in the bovine species.

Lack of a Direct Effect of 1,25-Dihydroxycholecalciferol on Parathyroid Hormone Secretion by Normal Bovine Parathyroid Glands*

Endocrinology ◽  
1980 ◽  
Vol 107 (2) ◽  
pp. 602-607 ◽  
Author(s):  
PAUL GOLDEN ◽  
ALLEN GREENWALT ◽  
KEVIN MARTIN ◽  
EZEQUIEL BELLORIN-FONT ◽  
RICHARD MAZEY ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Direct Effect ◽  
Hormone Secretion ◽  
Parathyroid Glands

Association of Polymorphic Alleles of the Calcium-Sensing Receptor Gene with Parathyroid Hormone Secretion in Hemodialysis Patients

Nephron ◽  
2000 ◽  
Vol 85 (4) ◽  
pp. 317-323 ◽  
Author(s):  
Shozo Yano ◽  
Toshitsugu Sugimoto ◽  
Michiko Kanzawa ◽  
Tatsuo Tsukamoto ◽  
Tetsuya Hattori ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Receptor Gene ◽  
Hormone Secretion ◽  
Hemodialysis Patients ◽  
Calcium Sensing Receptor ◽  
Calcium Sensing ◽  
Calcium Sensing Receptor Gene

Suppression of parathyroid hormone secretion in hemodialysis patients by a novel vitamin D analogue: 19-nor-1,25-dihydroxyvitamin D2

1998 ◽  
Vol 32 (4) ◽  
pp. S48-S54 ◽  
Author(s):  
F Llach ◽  
G Keshav ◽  
MV Goldblat ◽  
JS Lindberg ◽  
R Sadler ◽  
...  
Keyword(s):  
Vitamin D ◽  
Parathyroid Hormone ◽  
Hormone Secretion ◽  
Hemodialysis Patients ◽  
Vitamin D Analogue

scholarly journals Differences in the dynamics of parathyroid hormone secretion in hemodialysis patients with marked secondary hyperparathyroidism.

1995 ◽  
Vol 6 (5) ◽  
pp. 1371-1378
Author(s):  
A J Felsenfeld ◽  
A Jara ◽  
M Pahl ◽  
J Bover ◽  
M Rodriguez
Keyword(s):  
Parathyroid Hormone ◽  
Secondary Hyperparathyroidism ◽  
Serum Calcium ◽  
Hormone Secretion ◽  
Hemodialysis Patients ◽  
Basal Serum ◽  
Group I ◽  
The Difference ◽  
Pth Level ◽  
Uniform Group

Hemodialysis patients with predialysis intact parathyroid hormone (PTH) levels of more than 500 pg/mL are generally considered to have marked secondary hyperparathyroidism. Because the serum calcium level in these patients varies from low to high, it is not clear whether every hemodialysis patient with a PTH level > 500 pg/mL is part of a uniform group. The dynamics of PTH secretion in 21 hemodialysis patients with predialysis (basal) intact PTH levels > 500 pg/mL (range, 506 to 1978 pg/mL) has been evaluated. The basal/maximal PTH ratio, an indicator of the degree of relative PTH stimulation in the baseline state, was inversely correlated with the maximal PTH (r = -0.71), the basal serum calcium (r = -0.70), and the difference between the serum calcium at basal and maximal PTH (r = 0.81); the latter is the decrement in serum calcium from baseline necessary to maximally stimulate PTH. Because the basal PTH level appeared to be disproportionately influenced by hypocalcemia, the 21 patients were separated into two groups on the basis of the basal serum calcium (Group I < 9 mg/dL and Group II > 9 mg/dL). Basal PTH was not different between the two groups, even though maximally stimulated PTH (1,219 +/- 204 versus 2,739 +/- 412 pg/mL; P < 0.01) as induced by hypocalcemia and maximally suppressed PTH (217 +/- 37 versus 528 +/- 104; P = 0.05) as induced by hypercalcemia were less in Group I with the low basal calcium; moreover, the ratio of basal/maximal PTH was higher (73 +/- 6 versus 47 +/- 5%; P < 0.01) in Group I with the low basal calcium. These results suggest that the reason for a basal PTH > 500 pg/mL may be different among hemodialysis patients. In hypocalcemic patients, the low serum calcium appeared to be a major impetus for the high basal PTH level. In conclusion, (1) the maximally stimulated PTH appears to provide a better means of separating patients with marked secondary hyperparathyroidism than the basal PTH and (2) hemodialysis patients with basal PTH levels > 500 pg/mL may not be a uniform group.

Parathyroid hormone and extrarenal acid buffering

1980 ◽  
Vol 239 (6) ◽  
pp. F533-F538
Author(s):  
J. A. Arruda ◽  
V. Alla ◽  
H. Rubinstein ◽  
M. Cruz-Soto ◽  
S. Sabatini ◽  
...  
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Parathyroid Hormone ◽  
Chronic Renal Failure ◽  
Buffering Capacity ◽  
Parathyroid Glands ◽  
Blood Ph ◽  
Acid Buffering ◽  
Acid Load

The role of parathyroid hormone (PTH) on the extrarenal buffering of an acid load was examined during HCl infusion (5 meq x kg-1 x h-1) to bilaterally nephrectomized rats. Thyroparathyroidectomized (TPTX) rats replaced with PTH had significantly higher blood pH and HCO3 values than TPTX rats not infused with PTH. Administration of EDTA, in a dose shown to release PTH, was associated with a significant increase in buffering capacity in intact but not in TPTX rats. Colchicine, given in a dose capable of stimulating PTH release, was also associated with enhanced buffering capacity in intact but not in TPTX rats. In TPTX rats infused with acetazolamide and PTH, the hormone failed to enhance extrarenal buffering of an acid load. Animals with chronic renal failure, induced by infarction of the kidney, also had an enhanced capacity to buffer an acid load. This enhanced buffering capacity in chronic renal failure was abolished by TPTX. Acute renal failure induced by bilateral ureteral ligation was also associated with increased buffering only in the presence of parathyroid glands. These data demonstrated that PTH, from either an exogenous or endogenous source, enhances extrarenal buffering capacity of an acid load. Chronic and acute renal failure are associated with increased buffering capacity, which is dependent on the presence of parathyroid glands. The data suggest that this effect is mediated through carbonic anhydrase.

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