Abstract
Perivascular adipose tissue (PVAT) surrounds the exterior of blood vessels and releases numerous substances such as adiponectin which positively modulate blood vessel tone. In some cardiovascular diseases such as diabetes and high blood pressure, the function of PVAT changes and we speculate that oxidant stress may play a role in this change. PVAT has the ability to generate both superoxide and nitric oxide and these can combine rapidly under physiological conditions to form peroxynitrite (ONOO-). In disease states, the production of ONOO- may be increased and so its effect on the function of PVAT is of great interest. Consequently, we studied the effects of acute addition of the oxidant species ONOO- on vascular tone and production of adiponectin by mouse thoracic aortic PVAT. Murine PVAT was immunostained for nitrotyrosine, indicating that ONOO- is formed in the PVAT. Exogenous ONOO- significantly increased the anticontractile effect of PVAT via increased adiponectin content but had no effect on eNOS expression or phosphorylation. These results suggest that generation of ONOO- within PVAT may be an important regulatory mechanism which influences the activity of PVAT. The effect of chronic exposure to raised levels of ONOO- on PVAT function remains to be determined.
Highlights
Perivascular adipose tissue (PVAT) forms the outer layer of all blood vessels with the exception of the cerebral blood vessels and consists of varying proportions of white and brown adipocytes as well as stromal vascular cells
To demonstrate that PVAT has the capacity to generate the two species required for formation of ONOO−, we attempted to detect NO and superoxide within samples of mesenteric PVAT
In this paper we describe novel data showing the effects of an acute period of oxidant stress on the function of murine perivascular adipose tissue
Summary
Perivascular adipose tissue (PVAT) forms the outer layer of all blood vessels with the exception of the cerebral blood vessels and consists of varying proportions of white and brown adipocytes as well as stromal vascular cells. Our recent research has highlighted an important enzyme called AMP-activated protein kinase (AMPK) which is expressed ubiquitously and which may be involved in regulating release of PVAT-derived factors which reduce contractility of the blood vessel. In mice lacking one particular isoform of AMPK, (AMPKα1 knockout mice) the ability of the PVAT to reduce contractility of a large blood vessel, the aorta, was lost [1]. This was due to the PVAT in the knockout mice releasing much lower quantities of an adipocytokine called adiponectin. Adiponectin can induce relaxation of the blood vessel via actions on both the vascular smooth muscle cells in the medial layer of the vessel as well as actions on the endothelial cells which line the blood vessels and are in contact with the blood
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