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Reviews in Cardiovascular Medicine  2019, Vol. 20 Issue (3): 139-151     DOI: 10.31083/j.rcm.2019.03.522
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Store-operated calcium channels: Potential target for the therapy of hypertension
Sukhwinder K. Bhullar1, Anureet K. Shah2, Naranjan S. Dhalla1, *()
1 Institute of Cardiovascular Sciences, St. Boniface Hospital Albrechtsen Research Centre, Department of Physiology and Pathophysiology, Max Rady College of Medicine, University of Manitoba, Winnipeg, R2H 2A6, Canada
2 Kinesiology and Nutritional Science, California State University, Los Angeles, CA, 90032, USA
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Effective therapy of hypertension represents a key strategy for reducing the burden of cardiovascular disease and its associated mortality. The significance of voltage dependent L-type Ca2+ channels to Ca2+ influx, and of their regulatory mechanisms in the development of heart disease, is well established. A wide variety of L-type Ca2+ channel inhibitors and Ca2+ antagonists have been found to be beneficial not only in the treatment of hypertension, but also in myocardial infarction and heart failure. Over the past two decades, another class of Ca2+ channel - the voltage independent store-operated Ca2+ channel - has been implicated in the regulation and fine tuning of Ca2+ entry in both cardiac and smooth muscle cells. Store-operated Ca2+ channels are activated by the depletion of Ca2+ stores within the endoplasmic/sarcoplasmic reticulum, or by low levels of cytosolic Ca2+, thereby facilitating agonist-induced Ca2+ influx. Store-operated Ca2+ entry through this pivotal pathway involves both stromal interaction molecule (STIM) and Orai channels. Different degrees of changes in these proteins are considered to promote Ca2+ entry and hence contribute to the pathogenesis of cardiovascular dysfunction. Several blockers of store-operated Ca2+ channels acting at the level of both STIM and Orai channels have been shown to depress Ca2+ influx and lower blood pressure. However, their specificity, safety, and clinical significance remain to be established. Thus, there is an ongoing challenge in the development of selective inhibitors of store-operated Ca2+ channels that act in vascular smooth muscles for the improved treatment of hypertension.

Key words:  Store-operated Ca2+-channels      endoplasmic/sarcoplasmic Ca2+ stores      stromal interaction molecule      orai channels      hypertension therapy     
Submitted:  05 July 2019      Accepted:  22 August 2019      Published:  30 September 2019     
  • St. Boniface Hospital Research Foundation, Winnipeg, Canada
*Corresponding Author(s):  Naranjan S. Dhalla     E-mail:

Cite this article: 

Sukhwinder K. Bhullar, Anureet K. Shah, Naranjan S. Dhalla. Store-operated calcium channels: Potential target for the therapy of hypertension. Reviews in Cardiovascular Medicine, 2019, 20(3): 139-151.

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Table 1  Classification and Effects of Different Types of Ca2+-antagonists
Classification Antagonists Effects References
A. Dihydropyridines Amlodipine, Aranidipine, Azelnidipine, Barnidipine, Benidipine, Cilnidipine, Clevidipine, Efonidipine, Felodipine, Isradipine, Lacidipine, Lercanidipine,
Manidipine, Nicardipine, Nifedipine, Nilvadipine, Nimodipine, Nisoldipine,
Nitrendipine, Pranidipine
Reduce systemic vascular resistance and arterial pressure. Bangalore et al., 1994; Kurokawa et al., 1997; Remuzzi et al., 2002
B. Non-Dihydropyridines
a. Benzothiazepines Clenazem, Diltiazem Reduce arterial pressure Hofmann et al., 1999
b. Phenylalkylamines Gallopamil, Verapamil, Fendiline Reduce myocardial oxygen demand, reverse coronary vasospasm Dilmac et al.,2003; Hockerman et al., 1997
C. Non-selective Bepridil, Flunarizine, Fluspirilene, Fendiline, Mibefradil Treat epilepsy and neuropathic pain Scultety and Tamaskovits, 1991
D. Non-medical Ethanol Induce muscle relaxation Wang et al., 1994
Figure 1.  Schematic mechanism of store-operated Ca2+ entry pathways. ER-endoplasmic reticulum; SR-sarcoplasmic reticulum; PM-plasma membrane; SOCC-store-operated Ca2+ channel;STIM-Stromal interaction molecule.

Table 2  Pharmacological inhibitors of Store-operated Ca2+ Entry (SOCE)
SOCE Inhibitors Blockade Site References
A. Lanthanides: La3+ (lanthanum) ; Gd3+ (gadolinium) SOCC Orai Hoth and Penner, 1993; Tian et al.,2016; Xu et al., 2015
B. Imidazole compounds: SKF-96365;SKF 96465; econazole; miconazole Thapsigargin mediated SOCC Chung et al.,1994; Franzius et al.,1994; Hoth and Penner, 1993
C. Diphenylboronate compounds: 2-Aminoethyldiphenyl borate (2-APB) : 2-APB analogs- DPB162-AE and DPB163-AE (2-APB derivatives) Translocation of STIM puncta and STIM/Orai binding; Partially Orai channel DeHaven et al., 2008; Gregory et al., 2001; Iwasaki et al., 2001; Peinelt et al., 2008
D. Pyrazolecompounds: Bis (trifluoromethyl) (BTP1, BTP2 and BTP3) SOCE Sweeney et al., 2009
E. ML-9 Myosin light chain kinase (MLCK) Coalescence of STIM1 into puncta Smyth et al., 2008
F. Diethylstilbestrol (DES 18) -a synthetic estrogen agonist SOCE in mast cells and vascular smooth muscle cells Hoth and Penner, 1993; Ohana et al., 2009
G. Carboxyamidotriazole (CAI) Ca2+ dependent inactivation CRAC Rodland et al.,1997
H. RO2959 Human TCR mediated SOCE Chen et al., 2013
I. Linoleic acid: 18-C polyunsaturated fatty acid (PUFA) SOCE by affecting STIM1 oligomerization and subsequent STIM1/ORAI1 coupling Holowka et al., 2014
Figure 2.  Effects of store-operated Ca2+ entry antagonists. ER-endoplasmic reticulum; SR-sarcoplasmic reticulum; PM - Plasma membrane; STIM-Stromal interaction molecule.

Figure 3.  Involvement of Store-operated Ca2+ entry in the development of hypertension. STIM-Stromal interaction molecule; ER-endoplasmic reticulum; SR-sarcoplasmic reticulum.

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