Modulation of vascular reactivity by perivascular adipose tissue (PVAT)

Agabiti Rosei, C; Paini, A; De Ciuceis, C; Withers, SB; Greenstein, A; Heagerty, AM; Rizzoni, D

Abstract

Purpose of Review: In this review we discuss the role of perivascular adipose tissue (PVAT) in the modulation of vascular contractility and arterial pressure, focusing on the role of the renin-angiotensin-aldosterone system and oxidative stress/inflammation.
Recent Findings: PVAT possesses an relevant endocrine-paracrine activity, which may be altered in several pathophysiological and clinical conditions. During the last two decades it has been shown PVAT may modulate vascular reactivity. It has also been previously demonstrated that inflammation in adipose tissue may be implicated in vascular dysfunction. In particular, adipocytes secrete a number of adipokines with various functions, as well as several vasoactive factors, together with components of the renin-angiotensin system which may act at local or at systemic level. It has been shown that the anticontractile effect of PVAT is lost in obesity, probably as a consequence of the development of adipocyte hypertrophy, inflammation, and oxidative stress.
Summary: Adipose tissue dysfunction is interrelated with inflammation and oxidative stress, thus contributing to endothelial dysfunction observed in several pathological and clinical conditions such as obesity and hypertension. Decreased local adiponectin level, macrophage recruitment and infiltration, and activation of renin-angiotensin-aldosterone system could play an important role in this regards.

• Journal Article Type: Article
• Acceptance Date: Mar 29, 2018
• Online Publication Date: May 7, 2018
• Publication Date: May 7, 2018
• Deposit Date: Apr 3, 2018
• Publicly Available Date: May 7, 2019
• Journal: Current Hypertension Reports
• Print ISSN: 1522-6417
• Electronic ISSN: 1534-3111
• Publisher: Springer Verlag
• Volume: 20
• Issue: 44
• DOI: https://doi.org/10.1007/s11906-018-0835-5
• Publisher URL: https://doi.org/10.1007/s11906-018-0835-5
• Related Public URLs: https://link.springer.com/journal/11906