@article{
author = "Gao, Ge and Bai, Xiao-Yan and Xuan, Chao and Liu, Xiao-Cheng and Jing, Wen-Bin and Novaković, Aleksandra and Yang, Qin and He, Guo-Wei",
year = "2012",
abstract = "Background and Aims. Intracellular calcium regulation in endothelial cells depends on transient receptor potential channels (TRPs). Canonical TRPs (TRPCs) are now recognized as the most important Ca2+-permeable cation channels in vascular endothelium and TRPC3 channel is reported to play a role in vasodilation in animal vessels. However, little is known about the role of TRPCs in human arteries. We therefore tested the hypothesis that TRPCs play a role in human arteries. Methods. Cumulative concentration-relaxation curves to acetylcholine (-11 to -4.5 log M) were established in the human internal mammary artery (IMA) rings (n = 42) taken from 28 patients undergoing coronary artery bypass grafting in precontraction induced by U46619 (-8 log M) in the absence or presence of SKF96365 (10 mu mol/L) or Pyr3 (3 mu mol/L). Protein expressions of TRPC3 were determined by Western blot and immunohistochemistry staining. Results. The maximal relaxation induced by acetylcholine was significantly attenuated by the nonspecific cation channels inhibitor, SKF96365 (48.2 +/- 3.7 vs. 66.0 +/- 0.9% in control, p lt 0.01) or the selective TRPC3 blocker, Pyr3 (58.4 +/- 2.3% vs. 67.7 +/- 1.1% in control, p lt 0.01). Protein expression of TRPC3 was detected in human 1MA. Conclusions. TRPC3 exists and plays a role in the acetylcholine-induced endothelium-dependent relaxation in the human IMA. This study suggests that TRPC3 may be a potential new target in endothelial protection in patients with endothelial dysfunction such as in patients with coronary artery disease in order to improve the long-term patency of the grafting vessels.",
publisher = "Elsevier Science Inc, New York",
journal = "Archives of Medical Research",
title = "Role of TRPC3 Channel in Human Internal Mammary Artery",
volume = "43",
number = "6",
pages = "431-437",
doi = "10.1016/j.arcmed.2012.08.010"
}