Recent studies have revealed that the sympathetic nervous system is involved in bone metabolism. We previously reported that noradrenaline (NA) suppressed K+ currents via Gi/o protein-coupled alpha(1B-)adrenergic receptor (alpha(1B)-AR) in human osteoblast SaM-1 cells. Additionally, it has been demonstrated that the intracellular Ca2+ level (ICa2+](i)) was increased by NA via alpha(1B)-AR. In this study, we investigated the signal pathway of NA-induced [Ca2+], elevation by using Ca2+ fluorescence imaging in SaM-1 cells. NA-induced [Ca2+]; elevation was suppressed by pretreatment with a PLC inhibitor, U73122. This suggested that the [Ca2+; elevation was mediated by Gq protein-coupled alpha(1B)-AR. On the other hand, NA-induced [Ca2+](i) elevation was completely abolished in Ca2+-free solution, which suggested that Ca2+ influx is the predominant pathway of NA-induced [Ca2+]; elevation. Although the inhibition of K+ channel by NA caused membrane depolarization, the Ca2+]; elevation was not affected by voltage-dependent Ca2+ channel blockers, nifedipine and mibefradil. Meanwhile, NA-induced [Ca2+; elevation was abolished following activation of store-operated Ca2+ channel by thapsigargin. Additionally, the [Ce2+ elevation was suppressed by store-operated channel inhibitors, 2-APB, flufenamate, GdCl3 and LaCl3. These results suggest that Ca2+ influx through store-operated Ca(2+)channels plays a critical role in the signal transduction pathway of Gq protein-coupled alpha(1B)-AR in human osteoblasts. (C) 2013 Elsevier Inc. All rights reserved.