Journal
JOURNAL OF HYPERTENSION
Volume 27, Issue 4, Pages 782-790Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/HJH.0b013e328324ed86
Keywords
adipose tissue; angiotensin 1-7; aorta; nitric oxide; relaxation
Categories
Funding
- Heart and Stroke Foundation of Ontario, Canada
- Canadian Institutes of Health Research
- Canadian Hypertension Society
- Wake Forest University School of Medicine, North Carolina
- Bristol-Myers Squibb
- Takeda Pharmaceutical (Osaka, Japan) [CV 11974]
- Kyowa Hakko Co. Ltd. of Japan [HS-142-1]
Ask authors/readers for more resources
Objective Recent studies have demonstrated that perivascular adipose tissue (PVAT) releases vascular relaxation factor(s), but the identity of this relaxation factor remains unknown. Here, we examined if angiotensin 1-7 [Ang-(1-7)] is one of the relaxation factors released by PVAT. Method Morphological and functional methods were used to study aorta from adult Wistar rats. Results Immunohistochemical staining showed abundant presence of Ang-(1-7) in aortic PVAT. In vessels with PVAT removed but intact endothelium (PVAT - E+), contraction induced by phenylephrine was attenuated by preincubation with Ang-(1-7). PVAT - E+ vessels precontracted with phenylephrine showed a concentration-dependent relaxation response to Ang-(1-7), and this response was abolished by the removal of endothelium. Relaxation response induced by Ang-(1-7) was also prevented by Ang-(1-7) receptor (Mas) antagonist (A779), nitric oxide synthase inhibitor, and nitric oxide scavenger. Ang-(1-7) did not cause a relaxation response in aorta precontracted with KCI, and the relaxation response to Ang-(1-7) was also blocked by calcium-dependent potassium (K-Ca) channel blockers. Incubation of PVAT + E+ vessels with A779 or angiotensin-converting enzyme 2 inhibitor DX600 or angiotensin-converting enzyme inhibitor enalaprilat increased the contraction induced by phenylephrine. Transfer of donor solution incubated with PVAT + E+ vessel to recipient PVAT - E+ vessel caused a relaxation response. This relaxation response was abolished when donor vessels were incubated with DX600 or enalaprilat or when recipient vessels were incubated with A779. Conclusion Ang-(1-7) released by PVAT acts on the endothelium to cause the release of nitric oxide, and nitric oxide acts as a hyperpolarizing factor through K-Ca channels to cause relaxation of the blood vessel. J Hypertens 27:782790 (C) 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available