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Updated: Jun 11, 2026

Assessment of Human Adipose Tissue Microvascular Function Using Videomicroscopy
Published on: September 29, 2017
Endothelium-dependent relaxation factor released by perivascular adipose tissue
Robert M K W Lee1, Chao Lu, Li-Ying Su
1Department of Anesthesia, McMaster University, Hamilton, Ontario, Canada. rmkwlee@mcmaster.ca
Angiotensin 1-7 released by perivascular adipose tissue (PVAT) causes blood vessel relaxation. This peptide acts on the endothelium, releasing nitric oxide that relaxes vessels via potassium channels.
Area of Science:
- Vascular biology
- Adipose tissue research
- Cardiovascular pharmacology
Background:
- Perivascular adipose tissue (PVAT) releases factors that influence vascular tone.
- The specific identity of PVAT-derived vascular relaxation factors remains largely unknown.
- Angiotensin 1-7 (Ang-(1-7)) is a peptide with known vasoactive properties.
Purpose of the Study:
- To investigate whether Angiotensin 1-7 (Ang-(1-7)) is a relaxation factor released by perivascular adipose tissue (PVAT).
Main Methods:
- Utilized morphological and functional methods on Wistar rat aortas.
- Employed immunohistochemistry to detect Ang-(1-7) presence in PVAT.
- Assessed vascular responses to Ang-(1-7) in the presence and absence of PVAT and endothelium, using pharmacological inhibitors.
Main Results:
- Abundant Ang-(1-7) was found in aortic PVAT.
- Ang-(1-7) induced concentration-dependent relaxation in vessels with intact endothelium and PVAT, abolished by endothelium removal, Mas antagonist, nitric oxide synthase inhibition, or nitric oxide scavenging.
- Ang-(1-7) relaxation was dependent on calcium-dependent potassium (K(Ca)) channels and did not occur with KCl-induced contraction.
Conclusions:
- Angiotensin 1-7 (Ang-(1-7)) released by perivascular adipose tissue (PVAT) acts on the vascular endothelium.
- This interaction triggers the release of nitric oxide (NO).
- Nitric oxide functions as a hyperpolarizing factor via K(Ca) channels, mediating blood vessel relaxation.
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