Perivascular adipose tissue: more than just structural support

Abstract

PVAT (perivascular adipose tissue) has recently been recognized as a novel factor in vascular biology, with implications in the pathophysiology of cardiovascular disease. Composed mainly of adipocytes, PVAT releases a wide range of biologically active molecules that modulate vascular smooth muscle cell contraction, proliferation and migration. PVAT exerts an anti-contractile effect in various vascular beds which seems to be mediated by an as yet elusive PVRF [PVAT-derived relaxing factor(s)]. Considerable progress has been made on deciphering the nature and mechanisms of action of PVRF, and the PVRFs proposed until now are reviewed here. However, complex pathways seem to regulate PVAT function and more than one mechanism is probably responsible for PVAT actions in vascular biology. The present review describes our current knowledge on the structure and function of PVAT, with a focus on its role in modulating vascular tone. Potential involvements of PVAT dysfunction in obesity, hypertension and atherosclerosis will be highlighted.

Figure 1

Myograph tracing representative of isometric contractile force recordings in isolated rat mesenteric artery rings. Cumulative concentration response curve to endothelin-1 in the absence (above, black) and presence (below, red) of PVAT. The scale represents time in minutes (X axis) and force in mN (Y axis).

Figure 2

Effects of perivascular adipose tissue on VSMCs.

Figure 3

Alterations of PVAT structure and function during obesity and hypertension lead to decreased anticontractile effects of PVAT. Although similar imbalances in adipokine release and inflammatory events occur in PVAT during atherosclerosis, there appear to be no changes in contractile function.