title: Role of TRPC3 channel in human internal mammary artery.
abstract: OBJECTIVE
  Intracellular calcium regulation in endothelial cells depends on transient receptor potential channels (TRPs). Canonical TRPs (TRPCs) are now recognized as the most important Ca(2+)-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 μmol/L) or Pyr3 (3 μmol/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 <0.01) or the selective TRPC3 blocker, Pyr3 (58.4 ± 2.3% vs. 67.7 ± 1.1% in control, p <0.01). Protein expression of TRPC3 was detected in human IMA.
  
  
  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.
authors.affiliation: TEDA International Cardiovascular Hospital, Medical College, Nankai University, Tianjin 300457, China.
authors.forename: Ge
authors.initials: G
authors.lastname: Gao
authors.forename: Xiao-Yan
authors.initials: XY
authors.lastname: Bai
authors.forename: Chao
authors.initials: C
authors.lastname: Xuan
authors.forename: Xiao-Cheng
authors.initials: XC
authors.lastname: Liu
authors.forename: Wen-Bin
authors.initials: WB
authors.lastname: Jing
authors.forename: Aleksandra
authors.initials: A
authors.lastname: Novakovic
authors.forename: Qin
authors.initials: Q
authors.lastname: Yang
authors.forename: Guo-Wei
authors.initials: GW
authors.lastname: He
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D015153:Blotting, Western; D002121:Calcium Channel Blockers / Q000494:pharmacology; D001026:Coronary Artery Bypass; D004121:Dimethyl Sulfoxide / Q000494:pharmacology; D004576:Electromyography; D006801:Humans; D007093:Imidazoles / Q000494:pharmacology; D007150:Immunohistochemistry; D066298:In Vitro Techniques; D008323:Mammary Arteries / Q000187:drug effects / Q000502:physiology*; D050052:TRPC Cation Channels / Q000502:physiology*; D014664:Vasodilation / Q000187:drug effects
chemical_list: D002121:Calcium Channel Blockers; D007093:Imidazoles; D050052:TRPC Cation Channels; C104603:TRPC3 cation channel; C063159:1-(2-(3-(4-methoxyphenyl)propoxy)-4-methoxyphenylethyl)-1H-imidazole; D000109:Acetylcholine; D004121:Dimethyl Sulfoxide