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06:56
Isolation, Culture, and Adipogenic Induction of Stromal Vascular Fraction-derived Preadipocytes from Mouse Periaortic Adipose Tissue
Published on: July 21, 2023
Modulation of vein function by perivascular adipose tissue.
Chao Lu1, Ashley X Zhao, Yu-Jing Gao
1Smooth Muscle Research Program and Department of Anesthesia, Faculty of Health Sciences, McMaster University, Hamilton, Ontario, Canada.
European Journal of Pharmacology
|January 18, 2011
Summary
Perivascular adipose tissue (PVAT) attenuates venous contraction by releasing angiotensin 1-7. This peptide induces relaxation via endothelial nitric oxide release and potassium channel activation, revealing a novel mechanism for venous function modulation.
Area of Science:
- Physiology
- Vascular Biology
- Pharmacology
Background:
- Perivascular adipose tissue (PVAT) is known to modulate arterial function via perivascular-derived relaxation factors (PVRF).
- The specific role and underlying mechanisms of PVAT in regulating venous tone remained largely unexplored.
- Understanding PVAT's influence on veins is crucial for a comprehensive view of vascular homeostasis.
Purpose of the Study:
- To investigate the role of PVAT in modulating the contractile function of the inferior vena cava.
- To elucidate the specific mechanisms by which PVAT influences venous smooth muscle activity.
- To identify the potential perivascular-derived relaxation factors involved in venous PVAT function.
Main Methods:
- Functional assessment of isolated rat inferior vena cava rings with varying combinations of intact or removed PVAT and endothelium.
- Pharmacological characterization of contractile responses to phenylephrine, U 46619, and 5-hydroxytryptamine.
- Investigation of relaxation responses to angiotensin 1-7 (Ang-(1-7)) using receptor antagonists and assessment of transferable relaxation factors.
Main Results:
- PVAT significantly attenuated agonist-induced venous contraction.
- Angiotensin 1-7 induced endothelium-dependent relaxation, abolished by Mas receptor antagonists.
- PVAT released a transferable factor, identified as Ang-(1-7), which mediated relaxation through endothelial nitric oxide (NO) and voltage-dependent potassium (Kv) channels.
Conclusions:
- Venous PVAT plays a significant role in attenuating agonist-induced contractions.
- Angiotensin 1-7 is identified as a key perivascular-derived relaxation factor released by venous PVAT.
- PVAT-derived Ang-(1-7) induces venous relaxation via endothelial NO release and Kv channel activation, highlighting a novel regulatory pathway.
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