Role of the calcium-sensing receptor in parathyroid gland physiology

2004 ◽  
Vol 286 (6) ◽  
pp. F1005-F1011 ◽  
Author(s):  
Randolph A. Chen ◽  
William G. Goodman

The calcium-sensing receptor (CaSR) represents the molecular mechanism by which parathyroid cells detect changes in blood ionized calcium concentration and modulate parathyroid hormone (PTH) secretion to maintain serum calcium levels within a narrow physiological range. Much has been learned in recent years about the diversity of signal transduction through the CaSR and the various factors that affect receptor expression. Beyond its classic role as a determinant of calcium-regulated PTH secretion, signaling through the CaSR also influences both gene transcription and cell proliferation in parathyroid cells. The CaSR thus serves a broad physiological role by integrating several distinct aspects of parathyroid gland function. The current review summarizes recent developments that enhance our understanding of the CaSR and its fundamental importance in parathyroid gland physiology.

PLoS ONE ◽  
2013 ◽  
Vol 8 (9) ◽  
pp. e73816 ◽  
Author(s):  
Pamela Di Tomo ◽  
Caterina Pipino ◽  
Paola Lanuti ◽  
Caterina Morabito ◽  
Laura Pierdomenico ◽  
...  

Biomolecules ◽  
2018 ◽  
Vol 8 (3) ◽  
pp. 69 ◽  
Author(s):  
Gordon L. Klein

The aim of this mini-review is to discuss the role of calcium in the process of cytokine-mediated bone resorption in an effort to understand the role circulating calcium may play in the resorption of bone. The liberation of calcium and possibly phosphorus and magnesium by bone resorption may sustain and intensify the inflammatory response. We used a burn injury setting in humans and a burn injury model in animals in order to examine the effects on the bone of the systemic inflammatory response and identified the parathyroid calcium-sensing receptor as the mediator of increasing bone resorption, hence higher interleukin (IL)-1 production, and decreasing bone resorption, hence the lowering of circulating ionized calcium concentration. Thus, extracellular calcium, by means of the parathyroid calcium-sensing receptor, is able to modulate inflammation-mediated resorption.


2009 ◽  
Vol 10 (3) ◽  
pp. 282-288 ◽  
Author(s):  
Guerman Molostvov ◽  
Rosemary Bland ◽  
Daniel Zehnder

2016 ◽  
Vol 49 ◽  
pp. 44-51 ◽  
Author(s):  
Jennifer L. Owen ◽  
Sam X. Cheng ◽  
Yong Ge ◽  
Bikash Sahay ◽  
Mansour Mohamadzadeh

2005 ◽  
Vol 288 (4) ◽  
pp. H1756-H1762 ◽  
Author(s):  
Jacqueline Ohanian ◽  
Kelly M. Gatfield ◽  
Donald T. Ward ◽  
Vasken Ohanian

Myogenic tone of small arteries is dependent on the presence of extracellular calcium ([Formula: see text]), and, recently, a receptor that senses changes in Ca2+, the calcium-sensing receptor (CaR), has been detected in vascular tissue. We investigated whether the CaR is involved in the regulation of myogenic tone in rat subcutaneous small arteries. Immunoblot analysis using a monoclonal antibody against the CaR demonstrated its presence in rat subcutaneous arteries. To determine whether the CaR was functionally active, segments of artery (<250 μm internal diameter) mounted in a pressure myograph with an intraluminal pressure of 70 mmHg were studied after the development of myogenic tone. Increasing [Formula: see text] concentration ([Ca2+]o) cumulatively from 0.5 to 10 mM induced an initial constriction (0.5–2 mM) followed by dilation (42 ± 5% loss of tone). The dose-dependent dilation was mimicked by other known CaR agonists including magnesium (1–10 mM) and the aminoglycosides neomycin (0.003–10 mM) and kanamycin (0.003–3 mM). PKC activation with the phorbol ester phorbol-12,13-dibutyrate (20nM) inhibited the dilation induced by high [Ca2+]o or neomycin, whereas inhibition of PKC with GF109203X (10 μM) increased the responses to [Formula: see text] or neomycin, consistent with the role of PKC as a negative regulator of the CaR. We conclude that rat subcutaneous arteries express a functionally active CaR that may be involved in the modulation of myogenic tone and hence the regulation of peripheral vascular resistance.


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