Potassium stimulates parathyroid hormone release in the absence of extracellular calcium

Abstract. Influence of vasoactive intestinal polypeptide, neuropeptide Y, calcitonin gene-related peptide, and substance P was investigated on dispersed parathyroid cells of adult cattle. At a physiological concentration of extracellular calcium, vasoactive intestinal polypeptide stimulated the parathyroid hormone release in a dose-dependent manner, whereas no effects were noted for the other peptides. The dependency of PTH secretion upon extracellular calcium was shifted to the right by vasoactive intestinal polypeptide at 10−6 mol/l, with a tendency for greater effects at low (0.5 mmol/l) than high concentrations (2.0-3.0 mmol/l) of the cation. Vasoactive intestinal polypeptide significantly enhanced cAMP release of the parathyroid cells, whereas no influence was noted on cytoplasmic calcium or pH within the cells. The results suggest that vasoactive intestinal polypeptide stimulates the PTH release by interaction with cAMP production of the parathyroid cells. This effect may contribute to the development of hypercalcemia in patients with neuroendocrine tumours secreting vasoactive intestinal polypeptide.

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Prostaglandin F2αInhibits 3',5'-Adenosine Monophosphate Accumulation and Parathyroid Hormone Release from Dispersed Bovine Parathyroid Cells*

Endocrinology ◽

10.1210/endo-104-1-1 ◽

1979 ◽

Vol 104 (1) ◽

pp. 1-7 ◽

Cited By ~ 19

Author(s):

D. G. GARDNER ◽

E. M. BROWN ◽

R. WINDECK ◽

G. D. AURBACH

Keyword(s):

Parathyroid Hormone ◽

Adenosine Monophosphate ◽

Hormone Release ◽

Parathyroid Hormone Release

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

10.21203/rs.3.rs-205615/v1 ◽

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.

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