Yolanda Mendizábal1, Silvia Llorens, Eduardo Nava. 1. Area of Physiology, Department of Medical Sciences, University of Castilla-La Mancha, School of Medicine and Regional Centre for Biomedical Research (CRIB), Albacete, Spain.
Abstract
AIMS: We have studied the vasoactive role of prostaglandins derived from perivascular adipose tissue (PVAT) and their effects on endothelial function in healthy rats and rats with metabolic syndrome (SHROB). MAIN METHODS: Mesenteric resistance arteries (MRA) from SHROB and control rats (WKY) were mounted on wire myographs: a) together with a sphere of naturally occurring perivascular adipose tissue (with-PVAT group), or b) dissecting all the adventitial tissue (without-PVAT group). KEY FINDINGS: Endothelial function, tested by acetylcholine reactivity of SHROB arteries with PVAT, was significantly lower than that of WKY. With-PVAT arteries, especially the SHROB, showed lower responses than those without PVAT. NO synthase inhibition diminished the acetylcholine responses in every group except the with-PVAT SHROB group. Blockade of cyclooxygenase-2, PGI2-IP, TXA2-TP, or TXA2 synthase increased to different extents the arterial responses in the SHROB with-PVAT group. PVAT from both rat strains revealed cyclooxygenase-2 activity and immunoassay confirmed the release of PGE2, PGI2 and TXA2. SIGNIFICANCE: Our major finding is that PVAT is a source of vasoactive prostaglandins in WKY and SHROB. We also report that the presence of visceral PVAT causes endothelial dysfunction of resistance arteries in the SHROB. The vascular responses to prostaglandins partly underlie the endothelial dysfunction of SHROB arteries.
AIMS: We have studied the vasoactive role of prostaglandins derived from perivascular adipose tissue (PVAT) and their effects on endothelial function in healthy rats and rats with metabolic syndrome (SHROB). MAIN METHODS: Mesenteric resistance arteries (MRA) from SHROB and control rats (WKY) were mounted on wire myographs: a) together with a sphere of naturally occurring perivascular adipose tissue (with-PVAT group), or b) dissecting all the adventitial tissue (without-PVAT group). KEY FINDINGS: Endothelial function, tested by acetylcholine reactivity of SHROB arteries with PVAT, was significantly lower than that of WKY. With-PVAT arteries, especially the SHROB, showed lower responses than those without PVAT. NO synthase inhibition diminished the acetylcholine responses in every group except the with-PVAT SHROB group. Blockade of cyclooxygenase-2, PGI2-IP, TXA2-TP, or TXA2 synthase increased to different extents the arterial responses in the SHROB with-PVAT group. PVAT from both rat strains revealed cyclooxygenase-2 activity and immunoassay confirmed the release of PGE2, PGI2 and TXA2. SIGNIFICANCE: Our major finding is that PVAT is a source of vasoactive prostaglandins in WKY and SHROB. We also report that the presence of visceral PVAT causes endothelial dysfunction of resistance arteries in the SHROB. The vascular responses to prostaglandins partly underlie the endothelial dysfunction of SHROB arteries.
Authors: Nadia Ayala-Lopez; William F Jackson; Robert Burnett; James N Wilson; Janice M Thompson; Stephanie W Watts Journal: Am J Physiol Heart Circ Physiol Date: 2015-10-02 Impact factor: 4.733
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