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Mas receptors in modulating relaxation induced by perivascular adipose tissue

Item Type:Article
Title:Mas receptors in modulating relaxation induced by perivascular adipose tissue
Creators Name:Lee, R.M.K.W. and Bader, M. and Alenina, N. and Santos, R.A.S. and Gao, Y.J. and Lu, C.
Abstract:AIMS: 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. MAIN 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. KEY FINDINGS: 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. SIGNIFICANCE: 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.
Keywords:Mas Receptor, Perivascular Adipose Tissue, Relaxation, Endothelium, Animals, Mice
Source:Life Sciences
ISSN:0024-3205
Publisher:Pergamon Press (U.K.)
Volume:89
Number:13-14
Page Range:467-472
Date:26 September 2011
Official Publication:https://doi.org/10.1016/j.lfs.2011.07.016
PubMed:View item in PubMed

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