1. Adrenaline facilitates calcium channel currents in osteoblasts.
- Author
-
Uchida Y, Endoh T, Kobayashi H, Tazaki M, and Sueishi K
- Subjects
- 3T3 Cells, Adrenergic alpha-1 Receptor Antagonists pharmacology, Adrenergic beta-Agonists administration & dosage, Adrenergic beta-Antagonists pharmacology, Animals, Barium metabolism, Dose-Response Relationship, Drug, Epinephrine administration & dosage, Mice, Patch-Clamp Techniques, Prazosin pharmacology, Propranolol pharmacology, Signal Transduction drug effects, Adrenergic beta-Agonists pharmacology, Calcium Channels drug effects, Calcium Signaling drug effects, Epinephrine pharmacology, Osteoblasts drug effects
- Abstract
Adrenaline (Adr) is known to directly or indirectly modulate bone cell activity under physiological and pathological conditions. Osteoblasts play a major role in bone formation, employing intracellular Ca(2+) as a second messenger to modulate hormonal responses and as a cofactor for mineralization. Voltage-dependent Ca(2+) channels (VDCCs) mediate the influx of Ca(2+) in response to membrane depolarization. The purpose of this study was to investigate the effects of Adr on VDCC currents in osteoblasts using a patch-clamp recording method. Application of 1 mM Adr facilitated VDCC currents in a concentration-dependent manner. Pre-treatment with b receptor antagonist propranolol blocked Adr-induced facilitation of VDCC currents carried by Ba(2+) (IBa). These results indicate that Adr-induced facilitation of IBa was mediated by b receptors in MC3T3-E1 osteoblast-like cells. To our knowledge, the data presented here demonstrate for the first time that Adr facilitates VDCCs in MC3T3-E1 osteoblast-like cells.
- Published
- 2014
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