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Updated: Aug 9, 2026
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Assessment of Vascular Tone Responsiveness using Isolated Mesenteric Arteries with a Focus on Modulation by Perivascular Adipose Tissues
Published on: June 3, 2019
Perivascular adipose tissue and mesenteric vascular function in spontaneously hypertensive rats
Beatriz Gálvez1, Javier de Castro, Diana Herold
1Unidad de Cartografía Cerebral, Instituto Pluridisciplinar, Universidad Complutense de Madrid, Madrid, Spain.
Arteriosclerosis, Thrombosis, and Vascular Biology
|April 8, 2006
Summary
Perivascular adipose tissue in spontaneously hypertensive rats (SHR) has reduced function and mass compared to normotensive rats. This dysfunction may contribute to increased vascular resistance in hypertension.
Area of Science:
- Cardiovascular Physiology
- Adipose Tissue Biology
- Hypertension Research
Background:
- Perivascular adipose tissue (PVAT) in normotensive rats releases factors that induce vascular relaxation via voltage-dependent K+ (Kv) channels.
- The role of PVAT in the pathophysiology of hypertension remains largely unknown.
Purpose of the Study:
- To investigate potential differences in mesenteric PVAT mass and function between spontaneously hypertensive rats (SHR) and normotensive Wistar Kyoto rats (WKY).
- To assess the contribution of PVAT to vascular resistance in the context of hypertension.
Main Methods:
- Characterization of mesenteric bed (MB) weight, lipid content, and adipocyte size in WKY and SHR.
- Measurement of plasma lipids and leptin levels.
- Assessment of vascular function using isolated perfused mesenteric beds and artery rings, with Kv channel blockade using 4-aminopyridine (4-AP).
Main Results:
- SHR exhibited lower MB weight, lipid content, and smaller adipocytes compared to WKY.
- Kv channel blockade with 4-AP caused less increase in perfusion pressure and contractile effect in SHR compared to WKY.
- Anticontractile effects of PVAT were diminished in SHR mesenteric artery rings.
Conclusions:
- Visceral PVAT mass and function are reduced in SHR.
- These alterations in PVAT may contribute to the elevated vascular resistance characteristic of hypertension.
