Submitted on February 19, 2004
Accepted on June 9, 2004
Norepinephrine-induced calcium signaling and expression of adrenoceptors in avian tendon cells
Michelle E Wall1, James E Faber2, Xi Yang3, Mari Tsuzaki3, and Albert J Banes4*
1 Biomedical Engineering, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA; Orthopaedics, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA
2 Cell and Molecular Physiology, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA
3 Biomedical Engineering, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA
4 Biomedical Engineering, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA; Orthopaedics, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA; Research Department, Flexcell International Corp, Hillsborough, NC, USA
* To whom correspondence should be addressed. E-mail: ajbvault{at}med.unc.edu.
Sympathetic efferent nerves are present in tendons, but their function within tendon is unknown. 
1-Adrenoceptors are expressed by a variety of cell types. In the presence of norepinephrine (NE), adrenoceptors activate Gq/11 signaling pathways that, subsequently, increase intracellular calcium concentration ([Ca2+]ic). We hypothesized that avian tendon cells express functional adrenoceptors that respond to NE by increasing [Ca2+]ic. Avian tendon cells were analyzed for mRNA expression of 1-adrenoceptors by RT-PCR. Avian tendons expressed the 1A- and 1B-adrenoceptor subtypes. Furthermore, both tendon surface epitenon cells and internal fibroblasts infused with a calcium sensitive dye, fura-2, and stimulated with NE responded by increasing [Ca2+]ic. KMD 3213, an 1A-adrenoceptor antagonist, significantly reduced the Ca2+ response. Other adrenoceptor antagonists had no effect on the Ca2+ response. The absence of extracellular Ca2+ also significantly reduced the response to NE, indicating that Ca2+-influx contributed to the rise in [Ca2+]ic. This study provides the first evidence that tendon cells express adrenoceptors and that the NE-induced Ca2+ response is coupled to the 1A-adrenoceptor subtype.
