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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.

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Published on: September 29, 2017

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.