Abstract P463: Deterioration of Vasomotor Regulation of Perivascular Adipose Tissue at Later Stage of Metabolic Syndrome

Abstract

Obesity is a critical risk factor for metabolic syndrome, which increases development of cardiovascular complications. Perivascular adipose tissue (PVAT) is known to modulate vascular tone. We reported that PVAT increases vasodilation via enhancing endothelial nitric oxide production in mesenteric arteries of SHRSP.Z- Lepr fa /IzmDmcr rats (SHRSP.ZF) with metabolic syndrome (at 20 weeks of age; wks). However, the enhancing effects disappear at later stage (30 wks). We therefore investigated mechanisms underlying deterioration of the compensatory effects of PVAT in metabolic syndrome. Mesenteric arteries were isolated from male 20 and 30-week-old SHRSP.ZF, and vasodilation in response to nitroprusside was examined using bath bioassay techniques. Coexistence of PVAT from SHRSP.ZF at 20 wks increased vasodilation in arteries without PVAT from SHRSP.ZF at 20 wks, but the effects of PVAT were not substituted by replacement with PVAT from rats at 30 wks. Cyclic GMP levels in response to nitroprusside in arteries were increased by the presence of PVAT at 20 wks, but it was not altered by the presence of PVAT at 30 wks. In the presence or absence of vaspin, visfatin omentin, and apelin, vasodilation in response to nitroprusside was unchanged in SHRSP.ZF arteries at 20 wks. These results indicated that the production/release of diffusible vasodilator(s) from PVAT decreases with ageing. Vaspin, visfatin omentin, and apelin could be excluded from potential candidates of vasodilator(s). The deterioration of PVAT’s compensatory effects under the conditions of impaired vasodilations may induce cardiovascular complications at later stages of metabolic syndrome.