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ORIGINAL ARTICLE
Year : 2021  |  Volume : 64  |  Issue : 2  |  Page : 80-87

Characterization of Ca2+-Sensing Receptor-Mediated Ca2+ Influx in Microvascular bEND.3 Endothelial Cells


1 Department of Internal Medicine, Division of Cardiology, Kiang Wu Hospital, Macau, China
2 Cardiovascular Division, Fu Jen Catholic University Hospital, Fu Jen Catholic University, New Taipei City; Department of Cardiology, Lotung Poh-Ai Hospital, Yilan County, Taiwan
3 Department of Physiology, China Medical University, Taichung, Taiwan
4 VIP Department, East Hospital, Tongji University School of Medicine, Shanghai, China
5 Department of Anesthesiology, China Medical University Hospital; Department of Anesthesiology, Kuang Tien General Hospital, Taichung, Taiwan
6 Division of Cardiology, Department of Medicine, Wan Fang Hospital, Taipei Medical University, Taipei, Taiwan

Correspondence Address:
Prof. Yuk-Man Leung
Department of Physiology, China Medical University, Taichung
Taiwan
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/cjp.cjp_93_20

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Ca2+-sensing receptors (CaSR), activated by elevated concentrations of extracellular Ca2+, have been known to regulate functions of thyroid cells, neurons, and endothelial cells (EC). In this report, we studied CaSR-mediated Ca2+ influx in mouse cerebral microvascular EC (bEND.3 cells). Cytosolic free Ca2+ concentration and Mn2+ influx were measured by fura-2 microfluorometry. High (3 mM) Ca2+ (CaSR agonist), 3 mM spermine (CaSR agonist), and 10 μM cinacalcet (positive allosteric modulator of CaSR) all triggered Ca2+ influx; however, spermine, unlike high Ca2+ and cinacalcet, did not promote Mn2+ influx and its response was poorly sensitive to SKF 96365, a TRP channel blocker. Consistently, 2-aminoethoxydiphenyl borate and ruthenium red (two other general TRP channel blockers) suppressed Ca2+ influx triggered by cinacalcet and high Ca2+ but not by spermine. Ca2+ influx triggered by high Ca2+, spermine, and cinacalcet was similarly suppressed by A784168, a potent and selective TRPV1 antagonist. Our results suggest that CaSR activation triggered Ca2+ influx via TRPV1 channels; intriguingly, pharmacological, and permeability properties of such Ca2+ influx depended on the stimulating ligands.


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