Journal of Hypertension

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Journal of Hypertension:
doi: 10.1097/HJH.0b013e328324ed86
Original papers: Pathophysiological aspects

Endothelium-dependent relaxation factor released by perivascular adipose tissue

Lee, Robert MKW; Lu, Chao; Su, Li-Ying; Gao, Yu-Jing

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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 KCl, and the relaxation response to Ang-(1-7) was also blocked by calcium-dependent potassium (KCa) 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 KCa channels to cause relaxation of the blood vessel.

© 2009 Lippincott Williams & Wilkins, Inc.


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