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

1992 ◽  
Vol 263 (2) ◽  
pp. E195-E198 ◽  
Author(s):  
P. Schwarz ◽  
H. A. Sorensen ◽  
I. Transbol ◽  
P. McNair
Keyword(s):  
Steady State ◽  
Parathyroid Hormone ◽  
Hormone Secretion ◽  
Ionized Calcium ◽  
Intact Parathyroid Hormone ◽  
Hormone Release ◽  
Hormone Regulation ◽  
Clamp Technique ◽  
Baseline Concentration ◽  
Parathyroid Hormone Release

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.

Dopamine-stimulated parathyroid hormone release in vitro: further evidence for a two-pool model of parathyroid hormone secretion

1985 ◽  
Vol 63 (9) ◽  
pp. 1139-1144 ◽  
Author(s):  
David A. Hanley ◽  
Paul G. Wellings
Keyword(s):  
Parathyroid Hormone ◽  
Hormone Secretion ◽  
Parathyroid Tissue ◽  
Hormone Release ◽  
Low Calcium ◽  
Pool Model ◽  
Parathyroid Hormone Release ◽  
Perifusion System ◽  
Sustained Increase

Bovine parathyroid tissue was placed in an in vitro perifusion system for the study of parathyroid hormone secretion stimulated by low calcium and dopamine. Dopamine caused a transient increase in parathyroid hormone release, while low calcium caused a sustained increase in parathyroid hormone secretion. The dopamine response was similar to that caused by isoproterenol. After parathyroid hormone release had been stimulated by dopamine there was no response to isoproterenol, suggesting they cause the release of the same cellular pool of hormone. Inhibition of protein synthesis with cycloheximide eliminated the response to low calcium, with no effect on dopamine-stimulated parathyroid hormone release. These studies suggest dopamine stimulates the release of a limited quantity storage pool of parathyroid hormone, while low calcium causes a sustained release of hormone by stimulating secretion of newly synthesized hormone. Low calcium has little or no effect on release of the storage granule pool of parathyroid hormone.

Parathyroid hormone release from the perfused canine thyroid-parathyroid complex isolated in situ

1980 ◽  
Vol 93 (2) ◽  
pp. 186-189 ◽  
Author(s):  
Bjarne Bach Pedersen ◽  
Peter Laurberg ◽  
Merete Sanvig Christensen ◽  
Stig Pors Nielsen
Keyword(s):  
Parathyroid Hormone ◽  
Parathyroid Gland ◽  
Direct Measurement ◽  
Synthetic Medium ◽  
Ionized Calcium ◽  
Hormone Release ◽  
Free Medium ◽  
Parathyroid Hormone Release

Abstract. A model for direct measurement of hormone release from the canine parathyroid gland is described. The two separate thyroid-parathyroid gland complexes were isolated in situ and perfused independently using a synthetic medium with a welldefined concentration of ionized calcium (Ca++). The concentration of parathyroid hormone (PTH) in the effluent was measured by radioimmunoassay, using an antiserum to bovine PTH that cross-reacts with canine PTH. Displacement curves of dilutions of effluent samples were similar to those of bovine PTH (1–84). During infusion of 1.49 mmol/l Ca++ the PTH release was constant for more than 4 h. Variations in Ca++ from 1.56 to 1.15 or 2.15 mmol/l induced rapid and sustained stimulation or suppression of PTH release. The retained ability of the preparation was ascertained by recording the response to infusion of calcium free medium at the end of each experiment.

scholarly journals Effects of Orai3-Mediated Store-Operated Calcium Entry on Parathyroid Hormone Release in Secondary Hyperparathyroidism

2021 ◽  
Author(s):  
Zhangying Lin ◽  
Shuhao Wang ◽  
Yanxun Han ◽  
Junwei Zhu ◽  
Suwen Bai ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Parathyroid Hormone ◽  
Secondary Hyperparathyroidism ◽  
Tumor Development ◽  
Parathyroid Tissue ◽  
Hormone Release ◽  
Common Complication ◽  
Store Operated Calcium Entry ◽  
Serum Pth ◽  
Parathyroid Hormone Release

Abstract Secondary hyperparathyroidism (SHPT) is a common complication of chronic kidney disease, is characterized by elevated parathyroid hormone (PTH) secretion and Hypocalcemia. Orai3 is a highly selective calcium (Ca2+) channel that plays important roles in tumor development, cardiovascular disease, and autoimmune diseases; however, its role in SHPT is unclear. In the present study, RNA sequencing and western blot assays were used to detect the expression levels of Orai3 in parathyroid tissue from patients with SHPT and from individuals without SHPT. Ca2+ imaging was used to detect the effect of Orai3 channels on Ca2+ signaling in parathyroid gland cells. Enzyme-linked immunosorbent assays were used to detect changes in PTH release. Orai3 knockout rats were used to detect the effect of decreased Orai3 expression on serum PTH levels. We found that the expression of Orai3 in parathyroid tissue obtained from patients with SHPT was significantly higher than that in patients without SHPT. Knockdown of Orai3 in parathyroid cells by transfection with Orai3-specific small inhibitor RNA inhibited store-operated Ca2+ entry (SOCE) in parathyroid cells. Inhibition of SOCE or knockdown of Orai3 significantly inhibited PTH release in parathyroid cells. PTH levels in the blood of Orai3 knockout rat were significantly reduced. Therefore, Orai3 expression and Orai3-mediated Ca2+ signaling may be a mechanism underlying PTH release, and Orai3 may play a role in the development of SHPT.

Normalizing effect of Ca2+ ionophore on cytoplasmic Ca2+ and parathyroid hormone release of dispersed parathyroid cells from patients with hyperparathyroidism

1986 ◽  
Vol 45 (2-3) ◽  
pp. 191-196 ◽  
Author(s):  
Rolf Larsson ◽  
Chris Wallfelt ◽  
Göran Åkerström ◽  
Sverker Ljunghall ◽  
Jonas Rastad ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Hormone Release ◽  
Parathyroid Hormone Release

Functional dedifferentiation of parathyroid cells results both from a defective regulation and action of cytoplasmic Ca2+

1986 ◽  
Vol 6 (12) ◽  
pp. 1057-1063 ◽  
Author(s):  
Peter Nygren
Keyword(s):  
Parathyroid Hormone ◽  
Inhibitory Action ◽  
Monolayer Culture ◽  
Hormone Secretion ◽  
Dose Effect ◽  
Parathyroid Cell ◽  
Hormone Release ◽  
Parathyroid Adenomas ◽  
Small Inhibition

Monolayer culture of bovine parathyroid cells for 24 hours resulted in a right-shift of the dose-effect relationships for Ca2+-inhibition of parathyroid hormone (PTH) release and the dependence of the cytoplasmic Ca2+ concentration (Ca2+) on extracellular Ca2+ as well as in a less suppressible hormone release. After 4 days of culture, hormone secretion was almost non-suppressible and Cai2+ increased poorly in response to a rise in extracelluiar Ca2+. Ionomycin, a Ca2+ ionophore, raised Cai2+, but there was only a small inhibition of PTH release and the correlation between Cai2+ and secretion was weak. A deteriorated Cai2+ regulation and a decreased inhibitory action of cytoplasmic Ca2+ on PTH release were also found in ceils from human parathyroid adenomas. Functional dedifferentiation of the parathyroid cell thus results from both defective regulation and action of cytoplasmic Ca2+.

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