title: Mas receptors in modulating relaxation induced by perivascular adipose tissue.
abstract: OBJECTIVE
  Perivascular adipose tissue (PVAT) is known to secrete vascular relaxation factors, and angiotensin 1-7 [Ang-(1-7)] acting on the endothelium is one of the endothelium-dependent relaxation factors. Mas protein is the receptor for Ang-(1-7). Using aorta from Mas-knockout (K/O) and wild type (FVB) mice, we wished to establish the essential role of Mas receptors in mediating the endothelium-dependent relaxation response induced by relaxation factors from PVAT.
  
  
  METHODS
  Thoracic aortic rings from K/O and FVB mice were prepared with or without PVAT (PVAT+ and PVAT-) and/or intact endothelium (E+) or with the endothelium removed (E-) for functional studies. The contraction and relaxation responses of these vessels to agonist in the presence of different receptor antagonists were studied.
  
  
  RESULTS
  PVAT attenuated the contraction induced by phenylephrine (PHE) in the presence of endothelium only in vessels from FVB mice. Mas receptor antagonists D-Ala-Ang-(1-7) (A779) or D-Pro(7)-Ang-(1-7) enhanced the contraction induced by PHE only in vessels from FVB mice. Ang-(1-7) caused a relaxation response only in E+vessels from FVB mice. Transfer of donor solution from PVAT+ vessels to PVAT- recipient vessels caused a relaxation response among FVB vessels and not among vessels from K/O mice.
  
  
  CONCLUSIONS
  Mas receptors are essential in mediating the endothelium-dependent relaxation response induced by PVAT, therefore highlighting the important role of Ang-(1-7) in the control of vascular functions through PVAT.
authors.affiliation: Smooth Muscle Research Program and Department of Anesthesia, McMaster University, Hamilton, Ontario, Canada. rmkwlee@mcmaster.ca
authors.forename: Robert M K W
authors.initials: RM
authors.lastname: Lee
authors.forename: Michael
authors.initials: M
authors.lastname: Bader
authors.forename: Natalia
authors.initials: N
authors.lastname: Alenina
authors.forename: Robson A S
authors.initials: RA
authors.lastname: Santos
authors.forename: Yu-Jing
authors.initials: YJ
authors.lastname: Gao
authors.forename: Chao
authors.initials: C
authors.lastname: Lu
mesh_terms: D000273:Adipose Tissue / Q000378:metabolism*; D000803:Angiotensin I / Q000378:metabolism*; D000818:Animals; D001013:Aorta, Thoracic / Q000378:metabolism / Q000502:physiology*; D004730:Endothelium, Vascular / Q000378:metabolism; D051379:Mice; D018345:Mice, Knockout; D010446:Peptide Fragments / Q000378:metabolism*; D010656:Phenylephrine / Q000494:pharmacology; D011189:Potassium Chloride / Q000378:metabolism; D000090063:Proto-Oncogene Mas; D011518:Proto-Oncogene Proteins / Q000235:genetics / Q000378:metabolism*; D043562:Receptors, G-Protein-Coupled / Q000235:genetics / Q000378:metabolism*; D014662:Vasoconstrictor Agents / Q000494:pharmacology; D014664:Vasodilation
chemical_list: D010446:Peptide Fragments; D000090063:Proto-Oncogene Mas; D011518:Proto-Oncogene Proteins; D043562:Receptors, G-Protein-Coupled; D014662:Vasoconstrictor Agents; D010656:Phenylephrine; D011189:Potassium Chloride; D000803:Angiotensin I; C118790:angiotensin I (1-7)