期刊
JOURNAL OF HYPERTENSION
卷 27, 期 4, 页码 782-790出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/HJH.0b013e328324ed86
关键词
adipose tissue; angiotensin 1-7; aorta; nitric oxide; relaxation
资金
- 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]
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.
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